Magick and Melatonin

“The bird a nest, the spider a web,  man friendship.”

“Opposition is true friendship.”

William Blake 

Occult Oculus 

Melatonin is generally most associated with the Pineal gland where it is produced in most vertebrates. It is produced in many other tissues as well as being present in plants. It appears to be an ancient molecule occurring in unicellular organisms at a very early stage of Life.

Melatonin  is found in large amounts in the mitochondria the locus of energy generation within the cell, it has been suggested that it is in the mitochondria where it’s synthesis occurs.

The most simple pineal complex found in vertebrates,  that of the lamprey consists of foldings  of the diencephalic roof and has a retina like structure containing photoreceptor cells and secondary neurons. In more complex vertebrates the folding is multiplied (Vigh et al. 1998). The mammalian pineal gland itself is generally considered to be light insensitive, modern birds and reptile pineal glands contain the phototransducing pigment melanopsin.


The Pineal organ is located in the geometric centre of the brain in most mammals including humans where it is roughly the size of a grain of rice. Historically it has often been considered significant and in Yoga it is sometimes said to be the physical manifestation of Sahasrara chakra (the Crown).


Third ventricle in red

The Pineal gland while in the centre of the brain exists outside of the blood-brain barrier, located at the rear of the third ventricle and a portion of it is in direct contact with the cerebrospinal fluid (CSF) this explains the much higher levels of melatonin in CSF than in circulation. Tan et al. 2016 suggest that the pineal gland may play a role in the circulation of CSF as well as it’s generation.

The Pineal gland is highly vascularised multiple arteries deliver blood to this little organ. At least in rats the minimum rate of pineal blood flow per gram tissue exceeds that of most endocrine organs. The rate of pineal blood flow is 16 times higher than that of the average gram of tissue in rats.

Tan et al. 2016 suggest that this high rate of blood flow points to both a metabolically active gland and one with a secretory role. The Pineal anterior collecting vein has a constriction point before emptying, sphincters may be present here regulating blood flow within the gland, the increase in pressure might allow increased CSF and melatonin secretion. The tissue of the pineal gland may have a higher rate of filtration than the renal glomerulus (Tan et al. 2016).

Melatonin levels generally appear to decline during the day, because it’s synthesis occurs at night melatonin has been called the chemical expression of darkness. It may be involved in dreaming some people who have taken it as a supplement report vivid dreams.

Melatonin is an indolamine derived from tryptophan with serotonin as an intermediate. Short wavelength light in the blue end of the spectrum inhibits the activity of arylkylamine N-acetlytransferase the penultimate enzyme that converts serotonin to melatonin. Longer wavelength light in the red, orange, and yellow part of the spectrum does not appear to inhibit melatonin synthesis  (Wright et al. 2004). The light is believed to act via neural pathways from the retina through the suprachiasmatic nucleus to the pineal.

In addition to melatonin the pineal gland secretes other substances including the beta-carboline pinoline and the tetrapeptide epithalamin. The Pineal organ may also be a source of the potent psychedelic DMT though this is still unconfirmed, the related 5-MeO-DMT does seem to be found in human pineal gland and DMT does occur in small quantities in human cerebrospinal fluid (Smythies et al. 1979).

Damage to the pineal gland can result in precocious puberty,  premature development of the sex organs and skeleton.

Some bats appear to have unusually large pineal glands, relative to body mass the New Guinea naked backed bat Dobsonia praedatrix may have the largest pineal gland of any animal (Bhatnagar et al. 1990). The vampire Desmodus rotundus has a large pineal with complex structure and an ultrastructure unlike any other reported mammal.

Thorough Thaumaturgy 

Melatonin seems to have a wide range of beneficial actions many of  these seem to be a result of its antioxidant activity. Melatonin protects against gamma radiation, reducing rates of edema, necrosis, and neuronal degeneration  (Erol et al. 2004). In a study using blood from human volunteers melatonin decreased chromosome aberrations as a result of radiation exposure (Reiter et al. 1996). Melatonin protects from ultraviolet radiation, cells treated with melatonin showed increased survival rates and decreased formation of the lipid peroxide malondialdehyde (Ryoo et al. 2001). Melatonin inhibited lipid peroxide production and tissue damage as a result of mercury exposure  (Sener et al. 2003). Melatonin inhibits lipopolysaccharide induced nitric oxide activation (Escames et al. 2003).

2016-08-01 18.27.40

Do what thou wilt shall be the whole of the Law.

Melatonin  seems to exert multiple pro mitochondrial effects, promoting mitochondrial fusion and inhibiting mitochondrial fission  (Parameyong et al. 2013 and Pei et al. 2016). Melatonin promotes the activity of respiratory complexes I and IV, counteracting respiratory inhibition induced by potassium cyanide (Martin et al. 2002). In a mouse model of accelerated aging melatonin increased life span and improved mitochondrial function lowering lipid peroxidation  (Rodriguez et al. 2008).

Melatonin increases brown adipose tissue (BAT) fat tissue characterised by increased mitochondrial density, it is involved in heat production generally  increased levels occur in youth. BAT appears to be a characteristically mammalian tissue and has not been found to occur in the vast majority of other vertebrates. Melatonin also appears to increase the metabolic activity of BAT mitochondria and may play a role in weight regulation (Tan et al. 2011). Melatonin increased the expression of uncoupling protein UCP1 and PGC1A by up to 2 fold (Jimenez-Aranda et al. 2013). PGC1A is a human accelerated region involved in mitochondrial biogenesis and maintaining oxidative characteristics of muscle fibres promoting type 1 slow red postural fibres.

Given the centrality of energy generation in every aspect of biology melatonin should be expected to exert multiple protective effects on the organism there is evidence that this is so.

Melatonin protects against fibrosis in seemingly all tissues. Melatonin acts at all stages of fibrosis inhibiting injury of epithelial cells in the initial phase , reducing inflammatory cell infiltration and deposition of collagen (Hu et al. 2016). Melatonin also seems to be able to reverse fibrotic changes (Dominguez-Rodriguez et al. 2016).

Melatonin reduced cerebral edema in rats preserving the integrity of the blood-brain barrier  (Gorgulu et al. 2001). Reduces pulmonary edema  (Chen et al. 2015).

Melatonin appears to be therapeutic in cancer, reducing the number of prostate cancer cells, stopping cell cycle progression and inducing cellular differentiation  (Sainz et al. 2005). In neuroblastoma cancer cells melatonin produced greater neuritis outgrowth and more differentiated cells (Cos et al. 1996). Concentrations of melatonin corresponding to physiological levels present in human blood during the evening hours significantly inhibited by up to 78% cell proliferation in a breast cancer cell culture model (Hill and Blask 1988). Cells showed improved morphological characteristics with reduced nuclear swelling and disruption of mitochondria. Melatonin reduced invasiveness of cancer cells, inhibiting the effects of estradiol on cell adhesion and cell migration  (Cos et al. 1998).

Melatonin seems to be able to inhibit aromatase, which converts testosterone into estradiol  (Chottanapund et al. 2014).

In mice melatonin reverses age related thymic involution (Tian et al. 2001). The thymus is a lymphoid organ found in the chest behind the sternum and in front of the heart, it is where T cells a type of white blood cell mature, it is at its largest in children and generally shrinks from puberty onwards. Removal of the pineal gland in newborn rats resulted in disorganisation of the thymus and malignant transformation. The thyroid also showed tissue changes with increased deposition extracellular matrix  (Csaba and Barath 1975).

Melatonin also protects against the effects of snake venom, including cobras and vipers, Melatonin reduced haemorrhage,  muscle necrosis, damage to liver, kidneys and lungs, levels of nitric oxide, lipid peroxides, and inflammation  (Katkar et al. 2014, Moneim et al. 2015, Al-Sadoon et al. 2016).

Melatonin appears to have significant morphogenic effects removal of the pineal organ can produce scoliosis in chickens (Wang et al. 1998 and Turgut et al. 2005). In humans scoliosis appears to be associated with significantly lower melatonin levels (Machida et al. 1996 and Sadat-Ali et al. 2000).

Melatonin may be involved in tooth development as rat dental cells appear to express melatonin “receptors”(Kumasaka et al. 2010).

Melatonin stimulates synthesis of type 1 collagen in human bone cells in vitro (Nakade et al. 1999), bone strength is determined not only by bone mineral  density but also by the protein matrix woven into the bone including collagen and other proteins.

The Starchild skull amongst its unusual features appears to consist of a thin but super strong bone reinforced by protein fibres, might an enlarged or more developed Pineal organ and increased melatonin have played a role in these traits?


Alien or Elfin?

More on the Starchild skull here:

The Starchild skull a third perspective: Aromorphic Evolution?

Melatonin enhanced differentiation of mesenchymal stem cells into chondrocytes, increasing the size and GAG production of cartilage tissue (Gao et al. 2014).

Melatonin preserves the integrity of the blood-brain barrier and protects against hydrocephaly  (Turgut et al. 2007). Low melatonin is associated with hydrocephaly (Yamada et al. 1991).

Melatonin decreases with age and the pineal organ accumulates calcium and fluoride  (Luke 2001 and Kunz et al 1999).

Calcification of the pineal organ is associated with decreased melatonin production and Alzheimer’s disease, significantly more pineal tissue is calcified in Alzheimer’s than in other types of dementia (Mahlberg et al. 2008).

Courage Crowns 

Impaired nocturnal secretion of melatonin occurs in coronary heart disease (Brugger et al. 1995).

There is some evidence for a sort of cardio-pineal axis mediated by melatonin and the natriuretic peptides (ANP,  BNP, and CNP) secreted  by the heart, other substances and subtler interactions might also be involved.

2016-08-02 06.35.24

Love is the law, love under will.

Post infarction  (heart attack) long-term melatonin supplementation elevates expression of ANP (a heart hormone) from the left ventricle in rats (Sallinen 2008).

A small study using only 6 individuals found some evidence that ANP might increase melatonin, in two individuals serum melatonin levels doubled in response to ANP  (Lissoni  et al. 1990).

The Pineal gland also appears to contain CNP  (Middendorff et al. 1996). In the pineal gland the natriuretic peptides elevate cyclic GMP levels (Olcese et al. 1994).

The Pineal organ is highly vascularised richly supplied by blood vessels with one  of the highest rates of blood flow of any tissue (below that of the carotid body and maybe the kidney and thyroid) with such an extensive blood supply it seems inevitable that a relationship between the heart and pineal gland must exist.

As the pineal organ exists outside of the blood-brain barrier it might be especially easy to increase blood flow to it using inversions such as headstand and shoulderstand, meditation seems likely to be helpful. Yoga and meditation have been found to increase melatonin levels (Harinath et al. 2004).

Do what Thou wilt shall be the whole of the Law.

Love is the Law, Love under Will.


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Dominguez-Rodriguez A, Abreu-Gonzalez P, Piccolo R, Galasso G, Reiter RJ, (2016), Melatonin is associated with reverse remodeling after cardiac resynchronization therapy in patients with heart failure and ventricular dyssynchrony, International Journal of Cardiology, 221, pp.359-363.

Erol FS, Topsakal C, Ozveren MF, Kaplan M, Ilhan N, Ozercan IH, Yildiz OG, (2004), Protective effects of melatonin and vitamin E in brain damage due to gamma radiation, Neurosurgical review, 27(1), pp. 65-69.

Escames G, León J, Macías M, Khaldy H, Acuña-Castroviejo D, (2003), Melatonin counteracts lipopolysaccharide-induced expression and activity of mitochondrial nitric oxide synthase in rats, The FASEB Journal, 17(8), pp.932-934.

Gao W, Lin M, Liang A, Zhang L, Chen C, Liang G, Xu C, Peng Y, Chen C, Huang D, Su P, (2014), Melatonin enhances chondrogenic differentiation of human mesenchymal stem cells, Journal of pineal research, 56(1), pp.62-70.

Görgülü A, Palaoglu S, Ismailoglu Ö, Tuncel M, Sürücü MT, Erbil M, Klnç K, (2001), Effect of melatonin on cerebral edema in rats,  Neurosurgery, 49(6), pp.1434-1442.

Harinath K, Malhotra AS, Pal K, Prasad R, Kumar R, Kain TC, Rai L, Sawhney RC, (2004). Effects of Hatha yoga and Omkar meditation on cardiorespiratory performance, psychologic profile, and melatonin secretion, The Journal of Alternative & Complementary Medicine, 10(2), pp.261-268.

Hill SM, Blask DE, (1988), Effects of the pineal hormone melatonin on the proliferation and morphological characteristics of human breast cancer cells (MCF-7) in culture, Cancer research, 48(21), pp.6121-6126.

Hu W, Ma Z, Jiang S, Fan C, Deng C, Yan X, Di S, Lv J, Reiter RJ, Yang Y, (2016), Melatonin: the dawning of a treatment for fibrosis? Journal of pineal research, 60(2), pp.121-131.

Jiménez‐Aranda A, Fernández‐Vázquez G, Campos D, Tassi M, Velasco‐Perez L, Tan DX, Reiter RJ, Agil A, (2013), Melatonin induces browning of inguinal white adipose tissue in Zucker diabetic fatty rats, Journal of pineal research, 55(4), pp.416-423.

Katkar GD, Shanmuga Sundaram M, Hemshekhar M, Sharma DR, Sebastin Santhosh M, Sunitha K, Rangappa KS, Girish KS, Kemparaju K, (2014), Melatonin alleviates Echis carinatus venom‐induced toxicities by modulating inflammatory mediators and oxidative stress, Journal of pineal research, 56(3), pp.295-312.

Kumasaka S, Shimozuma M, Kawamoto T, Mishima K, Tokuyama R, Kamiya Y, Davaadorj P, Saito I, Satomura K, (2010), Possible involvement of melatonin in tooth development: expression of melatonin 1a receptor in human and mouse tooth germs, Histochemistry and cell biology, 133(5), pp.577-584.

Kunz D, Schmitz S, Mahlberg R, Mohr A, Stöter C, Wolf KJ, Herrmann WM, (1999), A new concept for melatonin deficit: on pineal calcification and melatonin excretion,  Neuropsychopharmacology, 21(6), pp.765-772.

Lissoni P, Pelizzoni F, Grugni G, Guzzaloni G, Mauri O, Archili C, Galli MA, Morabito F, (1990), Melatonin response to atrial natriuretic peptide administration in healthy volunteers, Journal of cardiovascular pharmacology, 16(5), pp.850-852.

Luke J, (2001), Fluoride deposition in the aged human pineal gland, Caries Research, 35(2), pp.125-128.

Machida M, Dubousset J, Imamura Y, Miyashita Y, Yamada T, Kimura J, (1996), Melatonin: a possible role in pathogenesis of adolescent idiopathic scoliosis, Spine, 21(10), pp.1147-1152.

Mahlberg R, Walther S, Kalus P, Bohner G, Haedel S, Reischies FM, Kühl KP, Hellweg R, Kunz D, Pineal calcification in Alzheimer’s disease: an in vivo study using computed tomography, Neurobiology of aging, 29(2)pp. 203-209.

Martı́n M, Macıas M, León J, Escames G, Khaldy H, Acuña-Castroviejo D, (2002), Melatonin increases the activity of the oxidative phosphorylation enzymes and the production of ATP in rat brain and liver mitochondria, The international journal of biochemistry & cell biology, 34(4), pp. 348-357.

Middendorff R, Maronde E, Paust HJ, Müller D, Davidoff M, Olcese J, (1996), Expression of C‐type natriuretic peptide in the bovine pineal gland, Journal of neurochemistry, 67(2), pp.517-524.

Moneim AE, Ortiz F, Leonardo-Mendonca RC, Vergano-Villodres R, Guerrero-Martínez JA, López LC, Acuna-Castroviejo D, Escames G, (2015), Protective effects of melatonin against oxidative damage induced by Egyptian cobra (Naja haje) crude venom in rats, Acta tropica, 143, pp.58-65.

Nakade O, Koyama H, Ariji H, Yajima A, Kaku T, (1999), Melatonin stimulates proliferation and type I collagen synthesis in human bone cells in vitro, Journal of pineal research,  27(2), pp.106-110.

Olcese J, Müller D, Münker M, Schmidt C, (1994), Natriuretic peptides elevate cyclic 3′, 5′-guanosine monophosphate levels in cultured rat pinealocytes: evidence for guanylate cyclase-linked membrane receptors, Molecular and cellular endocrinology, 103(1-2), pp.95-100.

Parameyong A, Charngkaew K, Govitrapong P, Chetsawang B, (2013), Melatonin attenuates methamphetamine‐induced disturbances in mitochondrial dynamics and degeneration in neuroblastoma SH‐SY5Y cells,  Journal of pineal research, 55(3), pp.313-323.

Pei H, Du J, Song X, He L, Zhang Y, Li X, Qiu C, Zhang Y, Hou J, Feng J, Gao E, (2016), Melatonin prevents adverse myocardial infarction remodeling via Notch1/Mfn2 pathway,  Free Radical Biology and Medicine, 97, pp.408-417.

Reiter RJ, Herman TS, Meltz ML, (1996), Melatonin and radioprotection from genetic damage: in vivo/in vitro studies with human volunteers, Mutation Research/Genetic Toxicology,  371(3), pp.221-228.

Rodríguez MI, Escames G, López LC, López A, García JA, Ortiz F, Sánchez V, Romeu M, Acuña-Castroviejo D, (2008), Improved mitochondrial function and increased life span after chronic melatonin treatment in senescent prone mice,  Experimental gerontology, 43(8), pp.749-756.

Ryoo YW, Suh SI, Mun KC, Kim BC, Lee KS, (2001), The effects of melatonin on ultraviolet-B irradiated cultured dermal fibroblasts. Journal of dermatological science, 27(3), pp.162-9.

Sadat-Ali M, Al-Habdan I, Al-Othman A, (2000), Adolescent idiopathic scoliosis. Is low melatonin a cause? Joint bone spine, 67(1), pp.62-64.

Sallinen P, Mänttäri S, Leskinen H, Vakkuri O, Ruskoaho H, Saarela S, (2008), Long‐term postinfarction melatonin administration alters the expression of DHPR, RyR2, SERCA2, and MT2 and elevates the ANP level in the rat left ventricle, Journal of pineal research, 45(1), pp.61-69.

Şener G, Şehirli AÖ, Ayanogˇlu‐Dülger G, (2003),  Melatonin Protects Against Mercury (II)‐Induced Oxidative Tissue Damage in Rats, Pharmacology & toxicology, 93(6), pp.290-296.

Sainz RM, Mayo JC, Tan DX, León J, Manchester L, Reiter RJ, (2005), Melatonin reduces prostate cancer cell growth leading to neuroendocrine differentiation via a receptor and PKA independent mechanism, The Prostate, 63(1), pp.29-43.

Smythies JR, Morin RD, Brown GB, (1979), Identification of dimethyltryptamine and O-methylbufotenin in human cerebrospinal fluid by combined gas chromatography/mass spectrometry, Biological psychiatry, 14(3), p. 549.

Tan DX, Manchester LC, Fuentes‐Broto L, Paredes SD, Reiter RJ, (2011), Significance and application of melatonin in the regulation of brown adipose tissue metabolism: relation to human obesity, Obesity Reviews, 12(3)pp. 167-188.

Tan DX, Manchester LC, Reiter RJ, (2016), CSF generation by pineal gland results in a robust melatonin circadian rhythm in the third ventricle as an unique light/dark signal, Medical hypotheses, 86, pp.3-9.

Tian YM, Li PP, Jiang XF, Zhang GY, Dai YR, (2001), Rejuvenation of degenerative thymus by oral melatonin administration and the antagonistic action of melatonin against hydroxyl radical‐induced apoptosis of cultured thymocytes in mice, Journal of pineal research, 31(3), pp.214-221.

Turgut M, Kaplan S, Turgut AT, Aslan H, Güvenç T, Çullu E, Erdoǧan S, (2005), Morphological, stereological and radiological changes in pinealectomized chicken cervical vertebrae, Journal of pineal research, 39(4), pp. 392-399.

Turgut M, Erdogan S, Ergin K, Serter M, (2007), Melatonin ameliorates blood–brain barrier permeability, glutathione, and nitric oxide levels in the choroid plexus of the infantile rats with kaolin-induced hydrocephalus, Brain research, 1175, pp.117-125.

Vígh B, Röhlich P, Görcs T, Fejér Z, Vígh‐Teichmann I, (1998), The pineal organ as a folded retina: immunocytochemical localization of opsins, Biology of the Cell, 90(9), pp. 653-659.

Wang X, Moreau M, Raso VJ, Zhao J, Jiang H, Mahood J, Bagnall K, (1998), Changes in serum melatonin levels in response to pinealectomy in the chicken and its correlation with development of scoliosis, Spine, 23(22), pp.2377-2381.

Wright HR, Lack LC, Kennaway DJ, (2004), Differential effects of light wavelength in phase advancing the melatonin rhythm, Journal of pineal research, 36(2) pp.140-144.

Yamada N, Iwasa H, Mori S, Kurokawa N, Fujimoto K, Kawashima K, Masuzawa T, (1991), Melatonin Secretion in Normal Pressure Hydrocephalus After Cerebral Aneurysm Rupture, Neurologia medico-chirurgica, 31(8), pp. 490-497.

Bats Bats Bats and Bioenergetics

“The Bat that flits at close of Eve

Has left the Brain that won’t Believe.”

William Blake 


Flying Freaks

Bats are the second most species rich and abundant mammals (rodents are the first). Bats are dispersed across every continent except Antarctica and make up 20% of all mammals, with over 12,000 species of bat worldwide.  Their order is labelled Chiroptera  (Hand-wing), and consists of two suborders Megachiroptera (mega bats) also known as Yinpterochiroptera and Microchiroptera (Microbats) or Yangochiroptera.

They are the only mammal capable of true flight. Their physiology has been tailored to flight , possessing highly flexible wings that can be folded so as to virtually disappear when not in use (Cheney et al. 2015).


Bat wing (Cheney et al. 2015).

These wings have thin muscle fibres running through them allowing the bat to fine tune wing shape for different situations, the underside of these wings is covered in fine hairs allowing the bat to sense air flow and respond appropriately. Different wing shapes occur in different species depending on their flight style, in general when compared to birds bats are better generalists, and demonstrate greater manoeuvrability than birds. Some species including Nectar feeding bats are capable of hovering flight though not quite with the extreme skill hummingbirds display.

Bats can even flip in flight “landing” to hang upside down, spend the day in torpor, and fall back into flight the next night.

Thundering Thoraxes 

The demands of flight have lead to some developments in bat physiology,  most obvious (other than wings) is the extreme development of their cardiopulmonary system necessary to support the intense metabolic demands of flight, flying is no easy thing.

During flight heart rate can reach up to 1000 beats per minute. Bat hearts have amongst mammals the highest mitochondrial density, even the flight muscle (pectoralis) of bats has a greater mitochondrial density than the heart of other mammals, the muscle fibres are finer than other mammals and have an extensive capillary supply. Bats have the largest lungs and heart of all mammals relative to body mass. Amongst bats relative heart size decreases with increasing body size, lung size remains isometric (Canals et al.2005).


Centurio senex / wrinkle-faced bat

The fine structure of bat lungs has undergone  development when compared with other mammal lungs. The structure has complexified with an increase in capillary density and finer alveoli allowing for increased respiratory exchange (Figueroa et al. 2007).

The surfactant of the bat’s lung also appears to differ somewhat from other mammals though it fits a meaningful trajectory. With bats having a very low ratio of cholesterol to disaturated phospholipids (DSP).

Surfactant is a complex mixture of phospholipids, neutral lipid (especially cholesterol) and proteins.

The ability to lower and vary surface tension in response to varying surface area is attributed to interactions between the disaturated PLs (DSPs) and other lipids including cholesterol and unsaturated PLs.

The function of the lungs involves the ability to shift volumes from inhalation to exhalation this is affected by surfactant composition.

It seems likely that upon expiration compression of the Surfactant results in a squeezing out of unsaturated PLs and cholesterol. The disaturated PLs can be tightly compressed together as a result of the full saturation of their carbon chain and greater hydrophobicity. Unsaturated PLs cannot pack as tightly due to their unsaturation and resulting shape, and  they are less hydrophobic which interferes with tight packing.

For the Surfactant to spread over the alveolar surface on inspiration the surfactant must be in a liquid crystalline state. DPPC (dipalmitoylphosphophatidylcholine) the main disaturated PL found in surfactant has a phase transition temperature of 41°C . A pure DPPC film would require a higher body temperature to function but in combination with other components such as cholesterol surfactant can function at lower temperatures. In multiple animals the ratio of cholesterol to DSP rises during Torpor and Hibernation (when metabolism and body temperature decrease) showing how surfactant composition responds to changes in metabolism and body temperature.

Other organisms have lower body temperatures than mammals and tend to experience greater fluctuations in temperature. They also have simpler lung structures, amphibians have simple sac like lungs, reptiles slightly more developed lungs but both lack the alveolar structures and diaphragm of mammal lungs. Birds support high metabolic rates with a different solution they have a small pair of parabronchial lungs connected to a series of air sacs, which act like bellows moving air through the lungs in one direction. The lungs consist of a series of tubes (parabronchi) from which emanate the rigid air capillaries, alongside blood capillaries allowing gas exchange.

As a result organisms with less intense metabolism have a higher cholesterol to DSP ratio. The more complex structure of mammalian lungs require greater flexibility in the surfactant.  The increased surface area means more efficient reduction in volume must occur during exhalation and the surfactant must spread easily over alveolar surface on inhalation.

Among mammals bats with their incredibly intense metabolism have the lowest cholesterol to DSP ratio, in some cases up to 15 times less than other mammals (Daniels and Orgeig 2003).

Polyunsaturated fats (both omega 6 and 3) cause lung edema and alveolar thickening (Wolfe et al. 2002). Their unsaturation makes them more prone to spontaneous oxidation and breakdown into various toxic byproducts, in organisms with intense oxidative metabolisms their presence may be a real problem. Dietary PUFAs  (polyunsaturated fatty acids) are capable of altering lung surfactant composition lowering saturated phospholipids and increasing polyunsaturated phospholipids. Impaired surfactant function is involved in acute respiratory distress syndrome and severe pneumonia both of which show lowered levels of saturated phospholipids and increased unsaturated PLs (Schmidt et al. 2001). Polyunsaturated fats interfere with respiration at every level from the lung to the cell. At least if you are warm blooded and wish to remain so it might be wise to avoid polyunsaturated oils.

Bats coordinate respiration with wing beat frequency, generally inhalation occurs on the downstroke,  exhalation on the up stroke (Suthers et al. 1972).  Yogis take note bats practice vinyasa, movement coordinated with the breath.

Fuel and Fire

Bats have  a great variety of dietary habits, including insectivores,  carnivores, frugivores, nectatavores, and of course the blood drinking sanguivore vampires. This would seem to indicate that a wide variety of diets can support intense metabolisms however amongst bats those who have the highest metabolism and the most energy demanding flight style are the nectatavores who like hummingbirds are capable of energetically demanding hovering flight though the bat may be capable of a slightly more energy efficient hovering style. The nectatavores don’t have the highest cephalisation of bats that appears to be found amongst some fruit eating species, carnivores, and the Vampires (maybe being a little monstrous benefits the brain).

If you compare the structure of fats and sugars you will see that fat is basically a chain of carbon and hydrogen however sugar comes premixed with oxygen. The chemical formula of glucose (and fructose) is C6H12O6. Carbon for carbon fat requires more oxygen from the air to be oxidised to carbon dioxide and water. This could be thought of as being like the difference between a flame where combustion occurs when the fuel is not already mixed with oxygen from the air and when the fuel is already mixed with oxygen producing a shorter hotter more intense flame.


Left most flame relatively oxygen poor and Fuel rich, reducing flame. Right most flame oxygen rich, oxidising flame.

It seems the most pristine plasma may come from things that are sweet like a child’s blood.

Infernal Immortality 

Could this creature cursed contribute to cancer’s cure,

Or teach us how to evermore endure?

The Rate of living theory is still believed by many despite an abundance of evidence that more Life results in more Life. The belief is that an increase in metabolism must inevitably mean increased production of ROS (reactive oxygen species), and a resulting increase in wear and tear on the organism. Bats have intense metabolisms and live remarkably long for animals of their size, generally larger species of animal live longer than smaller,  although smaller animals of a given species often live longer than their larger relatives for example small dogs live longer than big dogs. When corrected for body size bats are the longest living order of mammals.

The longest living bat on record is a 41 year old Brandt’s bat (Myotis brandti) from Siberia  (Podlutsky et al. 2005).


2016-05-04 08.20.45

Correlation between body mass and maximum lifespan in mammals. Myotis bats are shown as blue diamonds, and other mammals as dark circles. The Brandt’s bat is indicated by a red diamond (Seim et al. 2013).


It was believed that hibernation might explain the longevity but even non-hibernating species show great longevity

Mitochondria from bats show reduced rates of reactive oxygen species (ROS) generation with some species producing half the amount of non-flying mammals with lower metabolism (Bruet-Rossinni 2004).

Bats appear to be highly disease resistant, being infamous viral reservoirs, including Rabies and Ebola. Viral persistence in the absence of disease or pathology characterises the relationship between bats and viruses. And bats carry a lot of viruses, they positively pulse with pestilence.

This disease resistance is likely linked to their ability to fly or more precisely the metabolism that supports this. During flight bats metabolism increases enormously when compared to non-flying but otherwise active bats, this can be an up to 16 fold increase in metabolism, in rodents running to exhaustion metabolism increases 7 fold (O’Shea et al. 2014). Strains of mice bred for high metabolism show stronger immune responses, the intense metabolism required for flight will lead to increased circulation and increased activity of white blood cells, replicating some aspects of fever. The cyclical nature of the metabolic multiplication that occurs during flight and it’s decrease during daily dreaming may mean that pathogens are controlled and eliminated during activity while some survive during the bat’s torpor to persist to the next night. The lowered temperature of hibernation should inhibit replication of most mammalian pathogens.

The intense cardiovascular activity required to support this metabolism should be resulting in large amounts of circulating natriuretic peptides  (heart hormones) released when the heart is stretched. The natriuretic peptides increase phagocyte activity, phagocytosis (the process by which cells, usually immune cells, engulf and digest foreign material) decreases with aging (Boran et al. 2008). The natriuretic peptides also have significant anti-cancer activity (Vesely et al. 2007),  bats seem to be resistant to cancer, although it does sometimes occur, the metabolism that a bat must maintain to sustain flight likely makes the metabolic derangement characteristic of cancer highly unlikely to occur.

But the bat must fly fast, or plummet from the sky, and slowly sicken and die.

These observations that an intense metabolism supports a strong “immune system” seem to support an alternative way of thinking about immune function, where immunity to disease is a secondary result of processes whose primary function is in morphogenesis, the maintenance of the organism’s functioning and form, if the organism is engaged in such intense activity that all of its substance is actively metabolising then no space will be available for any parasites to take root.

Vampire Venom

This beast with Black banners was sliced and diced it’s glands were gouged and chemicals computed.

Now this beast has Red references so as not to be refuted.

Vampire bat saliva is a complex cocktail of chemicals composed of over 8000 different molecules (proteins and glycoproteins) many of theses are some form of anti-coagulant,  some are anti-microbial and some have other effects (Francischetti et al. 2013). Their purpose is to ensure blood flows from victim to vampire.


Desmodus rotundus (common vampire bat skull).

Some of the constituents include Desmoteplase (DSPA), Draculin, and desmolaris, I have seen some articles that treat Desmoteplase and Draculin as alternate names for the same chemical but they are separate molecules both have anti-coagulant effects (Low et al. 2013).

Desmoteplase is a protease plasminogen activator and causes fibrinolysis, breaking down blood clots. Desmoteplase appears a more effective anticoagulant than tpa (tissue Plasminogen Activator) and is thought to be promising in preventing and treating ischemic strokes.

Draculin is a glycoprotein and anticoagulant which inhibits some activated coagulation factors.

Desmolaris is an anticoagulant that binds kallikrein and reduces bradykinin inhibiting thrombus formation. It also has anti-inflammatory actions preventing increases in vascular permeability (Ma et al. 2013).

As a result of these properties various extracts of Vampire saliva have undergone trials for treatment of stroke.

However they might also have relevance in other conditions; including cancer where disordered clotting appears involved. Tissue factor (TF) is a glycoprotein that activates the clotting cascade, fibrinogen is cleaved into fibrin which polymerizes forming clots. Tissue factor is expressed by tumour cells it causes fibrin to deposit on circulating tumour cells trapping them in microvascular structures and promotes thrombosis, metastases and tumour growth (Kasthuri  et al. 2009).

Generally the intense metabolism of the bat promotes circulation and inhibits clotting through a variety of paths, carbon dioxide production from the intense metabolism may be one of the more elegant things to think about in this respect. Carbon dioxide acts as a vasodilator and promotes mast cell and platelet stability inhibiting the release of histamine and serotonin. Histamine and serotonin increase vascular permeability decreasing blood volume thickening the blood and promoting clotting.

Vampire saliva also contains CNP a natriuretic peptide (heart hormone) which increases heart rate and heart conductivity  (Springer et al. 2012), as well as increasing the strength of contraction (Beaulieu et al. 1997).

CNP is thought to be the ancestral natriuretic peptide with the other natriuretic peptides (including ANP and BNP) being generated from CNP in fishes far back in Creation’s Coil, although similar peptides occur in simpler organisms (Takei et al. 2011 and Inoue et al. 2003).

CNP also plays a morphogenic role specifically regulating bone growth (Mericq 2000).

Among higher vertebrates obligate blood feeding occurs in only three New World vampire bat species. These three vampires all diverged from a common insectivorous ancestor in a short evolutionary time, representing an enormous genetic development and required multiple coherent physiological changes including sensory, renal, secretory and of course dental (vampire bats have razor teeth).

To believe this occurred randomly is ridiculous.  Thankfully there appear to be scientists thinking about evolution in more coherent ways. Phillips and Baker (2015), suggest that vampire physiology developed by recruiting existing genes from other biological functions. One of these involves Entpd1, usually expressed in vascular endothelial cells and having anti-haemostatic properties. Two main processes appear to be involved exon  microdeletions, the removal of small sequences of a gene and alternative splicing, in which parts of a gene are put together differently, it occurs during gene expression and results in a single “gene” coding for multiple proteins as a result of different exons being included or excluded from the messenger RNA. It is thought that around 60% of human disease mutations involve splicing rather than mutations of the “coding” sequence (Bigas et al. 2005).

This suggests that evolution is an exploratory art that involves creativity and improvisation directed by the organism in responses to both changes in the environment and changes in the organism’s perception of itself and the environment.

Sinister Senses

The Bat blitzes through dark night,

Cares not for black or white,

So only does the Devil’s delight.

Bats have developed super senses that most other mammals lack, most famously the ability to see with their ears. By emitting a rapidly repeating ultrasonic series of squeals and squeaks and listening to the echos these creatures can fly in total darkness, even the wise Owl can’t do that let alone a silly Swan.


Townsend’s Big-Eared Bat

There is evidence that parallel genetic changes have occured in echolocating bats and dolphins again suggesting that something more meaningful than random chance is involved in genetic adaptation (Liu et al. 2010).

FoxP2 is a transcription factor implicated in development and neural control of oro facial coordination. Equivalents show almost no variation across vertebrates.  Humans and chimpanzees differ by two amino acids. In echolocating bats however FoxP2 appears to have undergone intense selection and demonstrates extreme diversity (Li et al. 2007).  Variations in FoxP2 in bats appear to be related to variations in bat species sonar. It’s seems possible that given its role in oro facial coordination  FoxP2  may play a role in the diversity these dwellers in darkness display in their faces. Interestingly FoxP2 is one of the genes that appears to diverge significantly from human in the Starchild skull.

FoxP2 seems to be involved in vocal learning in humans and seems to play a similar role in song birds, it might also be so in bats.Mutations in FoxP2 have been linked to developmental verbal dyspraxia (difficulty coordinating the muscle movements required for speech). FoxP2 is expressed in the brain and involved in neurogenesis and cortical development. FoxP2 is expressed in the heart and lung, in the lung it appears to be involved in alveolar development.

Bats also seem to be capable of magneto-reception (Wang et al.  2007), and make use of it to orient themselves, mole rats are also capable of magneto-reception, and like the bat they are unusually long-lived though different adaptations are likely involved in the mole-rat, high carbon dioxide levels seems like a possible connection, bats generate huge quantities as a result of their intense night life, Mole-rats likely maintain high carbon dioxide levels as a consequence of living in burrows. Bats that roost in caves may also be benefiting from increased carbon dioxide levels, depending on ventilation some cavernous ecosystems used by bats can contain 200 times the atmospheric concentration of carbon dioxide (Howarth and Stone 1990). I think based on  Ray Peat’s work that carbon dioxide might be a bio-electric doping agent increasing the conductivity of proteins and coherence of the organism, so playing a role in increasing subtle sensitivity.

Energy and Ecology 

i-0c7b87437e5d3dd6edfd1c3dde62628c-sucker footed bat 2-thumb-300x384-47574

Sucker-footed bat

Obviously a creature like the bat with an intense metabolism requires a fecund environment to provide for it. Increasingly it is being realised that bat numbers and diversity are indicators of ecosystem health, bats also contribute to maintaining complex ecosystems they pollinate flowers, spread seeds from fruit, and control insect numbers ensuring vegetation is not overwhelmed. Their ability to fly, while energetically demanding  also allows them to participate in more intense flows of energy transformation.  Bats depend on complex ecosystems and in turn enrich them, and in many areas their numbers are declining.

Wicked Waves

In this Dread Dark what is this thing?

Weaving winds with webbed wing.

It’s thorax Thunders a Gigas Gongs,

This Lich’s lantern is ultrasonic songs.

Merrily murders moonstruck moths,

This Ghoul’s Ghost is gay as Goths.

Infernally inverted in cryptic caverns cursed it conspires,

Time twisting Heart harnesses Hell’s fires.

Now know this terror to be true,

Vampire Venom flows through You.


Beaulieu P, Cardinal R, Page P, Francoeur F,  Tremblay J, Lambert C, (1997), Positive chrontropic and inotropic effects of C-type natriuretic peptide in dogs, AJP-Heart, 273 (4), pp. 19333-1940.

Bigas NL, Audit B, Ouzounis C, Parra G, Guido R, (2005), Are splicing mutations the most frequent cause of hereditary disease, FEBS Letters, 579 (9), pp.1900-1903.

Borán MS, Baltrons MA, García A, (2008), The ANP‐cGMP‐protein kinase G pathway induces a phagocytic phenotype but decreases inflammatory gene expression in microglial cells, Glia, 56(4), pp. 394-411.

Brunet-Rossinni AK  (2004), Reduced free-radical production and extreme longevity in the little brown bat (Myotis lucifugus) versus two non-flying mammals, Mechanisms of ageing and development, 125(1), pp.11-20.

Canals M, Atala C, Grossi B, Iriarte-Díaz J, (2005), Relative size of hearts and lungs of small bats. Acta Chiropterologica. 7(1), pp.65-72.

Cheney JA, Konow N, Bearnot A, Swartz SM, (2015), A wrinkle in flight: the role of elastin fibres in the mechanical behaviour of bat wing membranes, Journal of The Royal Society Interface, 12(106), p. 20141286.

Daniels CB and Orgeig S, (2003) Pulmonary surfactant: the key to the evolution of air breathing. Physiology, 18(4), pp. 151-157.

Figueroa D, Olivares R, Salaberry M, Sabat P, Canals M, (2007), Interplay between the morphometry of the lungs and the mode of locomotion in birds and mammals. Biological research, 40(2), pp. 193-201.

Francischetti IM, Assumpção TC, Ma D, Li Y, Vicente EC, Uieda W, Ribeiro JM, (2013), The “Vampirome”: transcriptome and proteome analysis of the principal and accessory submaxillary glands of the vampire bat Desmodus rotundus, a vector of human rabies, Journal of proteomics, 82, pp. 288-319.

Howarth FG, and Stone FD, (1990), Elevated carbon dioxide levels in Bayliss Cave, Australia: Implications for the evolution of obligate cave species, Pacific Science, 44(3), pp. 207-218.

Inoue K, Naruse K, Yamagami S, Mitani H,  Suzuki N,  Takei Y, (2003), Four functionally distinct C-type natriuretic peptides found in fish reveal evolutionary history of the natriuretic peptide system, Proceedings of the National Academy of Sciences, 100 (17), pp. 10079-10084.

Kasthuri RS, Taubman MB, and Mackman N,  (2009), Role of tissue factor in cancer, J Clin Oncol, 27 (29), pp. 4834-4838.

Li G, Wang J, Rossiter SJ, Jones G, Zhang S (2007) Accelerated FoxP2 Evolution in Echolocating Bats. PLoS ONE 2(9): e900.

Liu Y, Cotton JA, Shen B, Han X, Rossiter SJ, Zhang S, (2010), Convergent sequence evolution between echolocating bats and dolphins, Current Biology, 20 (2), pp. 53-54.

Low DH, Sunagar K, Undheim EA, Ali SA, Alagon AC, Ruder T, Jackson TN, Gonzalez SP, King GF, Jones A, Antunes A, (2013), Dracula’s children: molecular evolution of vampire bat venom, Journal of proteomics, 89, pp. 95-111.

Ma D, Mizurini DM, Assumpção TC, Li Y, Qi Y, Kotsyfakis M, Ribeiro JM, Monteiro RQ, Francischetti IM, (2013), Desmolaris, a novel factor XIa anticoagulant from the salivary gland of the vampire bat (Desmodus rotundus) inhibits inflammation and thrombosis in vivo, Blood, 122(25) pp.4094-4106.

Mericq V, Uyeda JA, Barnes KM, de Luca F, and Baron J,  (2000), Regulation of fetal rat bone growth by C-type natriuretic peptide and cGMP, Pediatric Research, 47(2), pp. 189-189.

O’Shea TJ, Cryan PM, Cunningham AA, Fooks AR, Hayman DT, Luis AD, Peel AJ, Plowright RK, Wood JL, (2014), Bat flight and zoonotic viruses, Emerg Infect Dis, 20(5), pp.741-745.

Phillips CD, and Baker RJ, (2015), Secretory gene recruitment in vampire bat salivary adaption and potential convergences with sanguivorous leeches, Frontiers in Ecology and Evolution, 3, p.122.

Podlutsky AJ, Khritankov AM, Ovodov ND, Austad SN, (2005), A new field record for bat longevity. The Journals of Gerontology Series A: Biological Sciences and Medical Sciences, 60(11), pp.1366-1368.

Schmidt R, Meier U, Yabut-Perez M, Walmrath D,  Grimminger M,  Seger W, Gunther A, (2001), Alteration of fatty acid profiles in different pulmonary surfactant phospholipids in acute respiratory distress syndrome and severe pneumonia. American journal of respiratory and critical care medicine. 163(1) pp.95-100.

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Springer J, Azer J, Hua R, Robbins C,  Adamcyzk A,  McBoyle S,  Bissell MB, Rose RA (2012), The natriuretic peptides BNP and CNP increase heart rate and electrical conduction by stimulating ionic currents in the sino atrial node and atrial myocardium following administration of guanylyl cyclase-linked natriuretic peptide receptors, Journal of Molecular and Cellular Biology, 52 (5), pp. 1122-1134.

Suthers RA, Thomas SP, Suthers BJ, (1972), Respiration,  wing-beat and ultrasonic pulse emission in an echolocating bat, Journal of Experimental Biology, 56, pp. 37-48.

Takei Y, Inoue K, Trajanovska S, Donald JA,  (2011), B-type natriuretic peptide (BNP) not ANP is the principle cardiac natriuretic peptide in vertebrates as revealed by comparative studies, General and Comparative Endocrinology, 171 (3), pp.258-266.

Vesely DL, Eichelbaum EJ, Sun Y, Alli AA, Vesely BA, Luther SL, Gower WR, (2007), Elimination of up to 80% of human pancreatic adenocarcinomas in athymic mice by cardiac hormones, In Vivo, 21(3), pp. 445-451.

Wang Y, Pan Y, Parsons S, Walker M, Zhang S, (2007), Bats respond to polarity of a magnetic field. Proceedings of the Royal Society of London B: Biological Sciences, 274(1627), pp. 2901-2905.

Wolfe RR, Martini WZ, Irtun O, Hawkins HK, Barrow RE, (2002), Dietary fat composition alters pulmonary function in pigs. Nutrition, 18(7), pp. 647-653.

Energy, Evolution and Eventually Even Effervescent Elves?

“Each stage of evolutionary history has its characteristic metabolic chemistry. By protecting and promoting mitochondrial respiration we are contributing to our own evolution.”

Ray Peat

Part 1: Mojo and Mitochondria.

Mitochondria are the organelles responsible for energy production in the cell, it is within the mitochondria where food, in the form of carbohydrates, fats and protein, is oxidised to produce energy. The metabolism of glucose involves a step that happens outside of the mitochondria and without the need for oxygen, glycolysis which converts glucose to pyruvate, pyruvate then enters the mitochondria, where it is converted to acetyl-CoA which then enters the citric acid (Krebs/TCA) cycle where it is oxidised producing carbon dioxide, and water, NADH, enters the electron transport chain and is oxidized to NAD+, in healthy cells there is a high ratio of NAD+ to NADH,  increased NADH is found in multiple diseases including diabetes and cancer. The citric acid cycle is the key pathway that is common to carbohydrate, fat and protein metabolism. For each molecule of glucose  2 ATP are produced during glycolysis, and around 30 molecules of ATP from the mitochondrial phases, in theory more ATP could be produced but some degree of uncoupling usually occurs. If there is a lack of oxygen or something inhibits mitochondria pyruvate will be fermented to lactate.

Mitochondria in addition to being the site of energy production have other roles, they are involved in hormone production and response, being the site where cholesterol is converted into protective steroid hormones such as pregnenolone, progesterone and DHEA. Mitochondria play roles in cell identity and differentiation. They can vary in size and shape from simple rod and elliptical structures to complex extensive interconnected networks in cells with high energy demands such as muscle cells of the heart and diaphragm. These variations in size, shape and location are all responsive to changes in demands placed on their cells. Their activity is involved in generating a formative field.

The extensive mitochondrial networks result from an increase in mitochondrial fusion, simpler mitochondrial structures from fission processes. A balance between fusion and fission is essential to cell function, imbalances in either direction can cause problems. Generally fission (fragmentation) of mitochondria results in a decrease in oxidative metabolism, increased fission is associated with cell division, dedifferentiation, apoptosis, lowered cytochrome oxidase (a fundamental respiratory enzyme), increased glycolysis, and a range of diseases including diabetes, Huntington’s, and cancer. Fission is increased by high glucose levels, perhaps as it allows for increased glycolysis and pyruvate uptake if sustained it seems likely to encourage the fermentation of pyruvate into lactate. Glucose deprivation enhances mitochondrial fusion.

Images showing mitochondrial networks in neurons from normal mice and mice used to model Huntington's:

Images showing mitochondrial networks in neurons from normal mice and mice used to model Huntington’s (transgenic BACHD): healthy evenly distributed mitochondria along dendritic branches in WT neurons, in BACHD neurons mitochondria are fragmented and rarefied, with deformed dendrites and less branching (Shirendeb et al.2012).

Increased Mitochondrial fusion is associated with increased oxidative respiration, increased cytochrome oxidase, increased cell differentiation and specialisation. Denervation and disuse of tissues increases fission, use increases mitochondrial fusion (Iqbal et al. 2013).

Mitochondrial volume and activity decrease with aging, (Ratel et al. 2008). Mammals have more mitochondria than reptiles as well as more active mitochondria, with these mitochondria taking up a greater volume of their cells, some mammals having a sixfold greater oxidative capacity than reptiles (Else and Hulbert 1981).

Part 2: Accelerated Adaptation.

“A proposed law of aromorphosis: that the retardation of the flow of energy in living systems tends toward a maximum; in animals this would imply a trend toward larger-brained, longer lived and probably warmer animals, having a higher energy charge.”

Ray Peat

Human Accelerated Regions (HARs) are segments of the human genome that are conserved extensively within vertebrate evolution but are strikingly different in humans (even when compared to chimpanzees). They were identified by Katherine Pollard and other researchers, 202 HARs were identified with 49 of them being considered highly significant. They are numbered according to their degree of difference from chimpanzee equivalents, HAR1 being the most different (Pollard et al. 2006). Their striking degree of difference suggests that they have undergone a particularly rapid evolution, suggesting that conventional ideas about evolution as a slow mechanical process may need to be reconsidered.

HAR20 codes for the protein peroxisome proliferator-activated receptor gamma co-activator 1-alpha (PGC-1A), this makes it unusual among the human accelerated regions (HARs) as most of the others are non-coding, they do not encode proteins, non-coding DNA has previously been described as junk DNA, it makes up 98.5% of the human genome.

PGC-1A both induces mitochondrial biogenesis (increasing mitochondrial volume, and creating new mitochondria), and modulates the composition and function of individual mitochondria.

PGC-1A was originally discovered in brown fat cells, brown fat contains more mitochondria than white fat, increased levels of BAT (brown adipose tissue) are found in children. PGC-1A can increase mitochondria in white adipose tissue converting it to brown or beige (intermediate between white and brown). Exposure to cold can increase PGC-1A.

PGC-1A increases mitochondrial mass and oxygen consumption, lowered mitochondrial function is involved in multiple diseases some of these may involve impaired PGC-1A including Huntington’s, Parkinson’s, Alzheimer’s, and amyotrophic lateral sclerosis (ALS).

PGC-1A can be increased by muscular activity especially endurance activity. PGC-1A both causes the conversion of type 2 fast white glycolytic fibres to type 1 slow red oxidative fibres, and is expressed at higher levels by type1 red oxidative fibres with increased mitochondrial density, extensive capillary supply and increased nerve supply (Lin et al. 2002). Type 1 fibres are those fibres that are involved in maintaining body posture as their constant activity requires intense respiratory support, type 2 fibres are capable of exerting more explosive force but they lack the fine motor control of type 1. An increased ratio of type 1 to type 2 fibres is present in humans compared to our primate relatives.

More on muscle and metabolism here:

Muscle, metabolism, mitochondria and metamorphic mutation Magick

PGC-1A increases oxidative metabolism but lowers reactive oxygen species production (ROS) inducing the expression of ROS lowering enzymes (Austin and St. Pierre 2012).

PGC-1A increases UCP1 and mitochondrial uncoupling, uncoupling is an incompletely understood phenomenon where oxidative metabolism and oxygen consumption is uncoupled from ATP production, it is sometimes considered a wasteful process but it appears to be beneficial. One of the main sites of uncoupled respiration is brown fat where it acts to increase heat production, however heat production might not be it’s main function as often a significant amount of respiratory energy (in rats 20-25%) goes into uncoupling (Brand 2000). Uncoupling may also increase longevity, mice with the highest metabolism, most uncoupling had 17% higher oxygen consumption used 30% more energy and lived 36% longer than mice with the lowest metabolism (Speakman et al. 2004). Uncoupled mitochondria produce increased carbon dioxide as a result of their increased oxygen consumption.

Uncoupling is neuroprotective, protecting against excitotoxicity and reducing damage in the cortex by around 50% after traumatic brain injury (Maragos and Korde 2004).

Predictably mammals have more mitochondrial uncoupling than reptiles (Akhmerov 1986).

Uncoupling is associated with increased mitochondrial fusion ( Golic et al. 2014). PGC-1A promotes the expression of Mfn2 a protein involved in mitochondrial fusion.

Uncoupling increases mitochondrial oxygen consumption and lowers ROS, I think this supports the idea that oxidative metabolism is in some sense like a whirlwind, potentially self-intensifying. An increased metabolism coheres the respiratory apparatus, electrons (energy) travels through it without escaping to react inappropriately as might happen when less intense producing ROS. Alternatively the intense metabolism could be likened to a fierce flame burning bright without smoke, a less intense metabolism would be like a faint flame forming filthy fumes.

The increased carbon dioxide produced by uncoupled mitochondria dilate blood vessels assisting in bringing increased blood flow and oxygen, generally acts to protect proteins from oxidation and increase the coherence of the organism (Ray Peat has written extensively on the biology of carbon dioxide, there are a couple of articles on this site also).

The natriuretic peptides released by the heart when it is stretched by increased blood flow act in part by increasing PGC-1A (Engeli et al. 2012).

More on the natriuretic peptides here:

Heart hormones, Inversions and Immortality

Deletion of PGC-1A  results in vascular aging and atherosclerosis as well as decreasing telomerase reverse transcriptase (TERT), telomere shortening is involved in DNA damage, mitochondrial dysfunction, multiple diseases and general aging. TERT maintains telomere length, telomeres are the regions at the ends of chromosomes that protect the chromosome from deterioration or fusing with neighbouring chromosomes. Telomeres shorten during cell division. PGC-1A increases TERT, restoring telomere length ( Xiong et al. 2015). *BANG* What was that sound? Oh I think that was the final nail in the coffin of the Hayflick limit.

Low PGC-1A appears to be involved in multiple neurodegenerative diseases, including Diabetes, Alzheimer’s, Parkinson’s, Huntington’s and ALS, increasing PGC-1A appears to be protective and therapeutic against neurodegeneration, PGC-1A increases neuronal mitochondrial biogenesis, and nerve tissue like all highly metabolic tissues usually produces high levels of PGC-1A, thought, perception, intelligence and sensitivity are all dependent on energy.

As mentioned earlier most of the human genome consists of noncoding DNA, less than 2% encodes proteins, the majority of the Human Accelerated Regions (HARs) are noncoding DNA which is transcribed into non-coding RNA, clearly the “junk DNA” has purpose.

HAR1 is the most accelerated region, in humans it differs from the chimpanzee equivalent by 18 substitutions. The chimpanzee differs from the chicken equivalent by only 2 out of 118 bases (Pollard et al. 2006).

Human and chimpanzee skulls. Image credit D Roberts.

Human and chimpanzee skulls.
Image credit D Roberts.

In humans the RNA produced from HAR1 assumes a clover leaf like formation, in chimps a simpler hairpin like structure, the chimp and human HAR1 also have differing electro-phoretic mobility (Beniaminov et al. 2008).

Exactly how HAR1 functions is unknown, it is expressed in developing human and primate brains, with its expression pattern matching that of the extracellular matrix glycoprotein Reelin. Both HAR1 and Reelin are expressed primarily by Cajal-Retzius cells during development. HAR1 is also expressed in the testes and ovaries.

Reelin’s primary function appears to be in regulating the development of the cortex of the brain, guiding neuronal cell migration and positioning. Modulating synaptic plasticity and stimulating dendrite development. Decreased Reelin is implicated in schizophrenia, autism, Alzheimer’s, and temporal lobe epilepsy. A total lack of reelin results in the condition of lissencephaly, a smooth brain completely lacking the normal extensive gyrification (the cortical convolutions) of the human brain, resulting in profound cognitive impairment. Lissencephaly often occurs with hypotonia and a lack of unsupported sitting.

As evolution advances and the cortex becomes more complex Reelin expression goes up with human brains expressing the most. In mammals the cortex develops from inside to out producing a multilayer cortex, in reptiles the cortex develops outside to inside producing a single layer cortex (Molnar 2007).

Reelin appears to structure the space for cortical growth, supplementing mice with Reelin enhanced cognitive abilities, synaptic plasticity and dendritic spine density (Rogers et al. 2011). Reelin can also be increased through T3 the active thyroid hormone (Sui et al. 2010).

Reelin’s role as a morphogenic regulator is supported by decreased Reelin expression in cancer, with lowered reelin promoting the migration and invasion of cancer into surrounding tissues (Walter and Goggins 2008). Heme-oxygenase-1 a stress inducible protein responsible for the breakdown of heme, producing carbon monoxide and bile pigments, Carbon monoxide is a respiratory toxin and increased heme-oxygenase damages mitochondria and reduces reelin content of the brain, producing schizophrenia like symptoms, heme-oxygenase is also involved in cancer (Song et al. 2012).

Human Accelerated Regions, especially the top five show a strong bias for adenine and thymine substitution to guanine and cytosine suggestive of a directionality, a similar substitution of adenine and thymine for guanine and cytosine has been found in mitochondrial DNA to correlate with increased longevity (Lehmann et al. 2008).

I think the Human Accelerated Regions are highly suggestive that Lamarck was correct acquired characteristics can be inherited, meaning evolution is not some blind mechanical process that acts upon insensate dead matter, that it is essentially a living sensitive capacity of life. There is evidence that this is the case, Barbara McClintock experimenting with maize plants found that when the plants chromosomal ends (telomeres) were damaged, the cell appeared to be able to sense the damage and bring together the ruptured ends of chromosomes. If only a single (rather than a pair) chromosomal end is damaged repair is made more difficult, McClintock found that the cell would make use of mobile genetic elements that could repair the damage and restructure the genome at various levels. This suggests that the genome is not some inert structure mutating randomly, but capable of at least some degree of sensitivity adapting to challenges in a coherent non-random way (McClintock 1983).

John Cairns studying E.coli that were unable to metabolize lactose, found they were able when grown in media in which lactose was the only source of food to generate the necessary mutation to metabolize the lactose and survive. The rate of evolution was orders of magnitude higher than random chance would allow (Cairns and Foster 1991).

Part 3: Even Effervescent Elves.

“If we optimize the known factors which improve energy production (red light, short-chain and medium-chain saturated fats, and pregnenolone, for example), to the extent that our metabolism resembles that of a ten year old child, I don’t think there is any reason to suppose that we wouldn’t have the regenerative and healing abilities that are common at that age. I suspect that both brain growth and remodeling might proceed indefinitely.”

Ray Peat

I’ve written about the starchild skull previously:

The Starchild Skull a third perspective: Aromorphic Evolution

Alien or Elfin?

Alien or Elfin?

The Starchild may represent an early example of some of the evolutionary potential that is available to humans if we can reorient ourselves to a more sensitive understanding of the nature and possibilities of Life.

X-ray of Starchild Skull

X-ray of Starchild Skull

Our biology (biopsychology) is far more mutable and plastic than the dominant cult of genetic determinism supposes. This has been realised by multiple cultures and subcultures, the various spiritual systems at their core are attempts to promote our highest possibilities. Of course corruption co-option and confusion have occurred over time with some developing into authoritarian control systems that have stifled creativity, imagination and evolution producing sick psychic mono-cultures. Even then the core has usually remained intact.

Elongated skull from Paracas Peru. Brien Foerster has some interesting videos of similar skulls on youtube.

Elongated skull from Paracas Peru. Brien Foerster has some interesting videos of similar skulls on youtube.

The elongated skulls found worldwide may represent attempts to actively shape development, changing brain morphology possibly to emphasise certain capacities, these would have involved use of things such as head binding, perhaps these changes in brain morphology produced accumulated epigenetic modifications allowing for after a few generations some of the skulls which appear to have unusually large cranial volumes. The Starchild appears to have a more balanced morphology, and increased neoteny (youthful qualities), and may have occurred as a result of internal modifications rather than external.

Casts of inside of human skull (left) and starchild skull (right).

Casts of inside of human skull (left) and starchild skull (right). The casts don’t display the degree of gyrification due to the presence of protective layers between brain and skull, dura, arachnoid, subarachnoid space and pia mater.

Inner skull cast side view. Human left. Starchild right.

Inner skull cast side view. Human left. Starchild right. The Starchild appears to have a more developed cortex (Elves get Int and Dex bonuses, yes I played Dungeons and Dragons).

Brain regions. Frontal Lobe: Personality, concentration, planning problem solving, meaning, speech, smell. Parietal Lobe:touch, taste, proprioception, sensory combination and comprehension. Occipital Lobe: vision. Temporal lobe: hearing, facial recognition, emotion, memory. Cerebellum: balance and coordination.

Brain regions.
Frontal Lobe: Personality, concentration, planning problem solving, meaning, speech, smell, imagination.
Parietal Lobe:touch, taste, proprioception, sensory combination and comprehension, imagination.
Occipital Lobe: vision, imagination.
Temporal lobe: hearing, facial recognition, emotion, memory, imagination.
Cerebellum: balance, coordination, imagination.

The Starchild’s large cranial capacity is suggestive of an intense metabolism, as cephalisation (the relative enlargement of the head and the concentration of the nervous system within the head) in animals proceeds so does metabolic rate. The composition and quality of the Starchild’s bone also suggests an intense metabolism, relative to human bone it is thinner but apparently more durable, being woven through and strengthened by protein (collagen?) fibres, it’s increased carbon  content might result from an increased metabolism generating more carbon dioxide, allowing for a change and developmental advance in bone quality. Hypothyroidism (a decreased metabolism) is associated with increased fracture risk and weaker bones. Reptiles have more developed bones than amphibians and mammals still more so resulting not only from metabolic differences, but an increase in the complexity of the forces acting on the bones as a result of increasing nervous system development, mammals generally being more graceful than reptiles.

Cephalisation as an evolutionary trend in animals obviously goes along with increased self-awareness and reflective ability, simpler animals, fish, amphibians, and reptiles, appear to have relatively limited self-awareness, their awareness and energy is focused outwards on basic survival. If function produces structure, then cultivating internal sensitivity, reflective thought, and imagination should assist in developing those structures that support their function.

There are suggestions that conscious awareness can itself intensify metabolism meditators have lower lactate levels suggesting improved oxidative metabolism, denervation increases glycolysis and lactate production,  consciousness here appears like a self-intensifying process.

Clear links exist between mitochondrial energy status and gene expression, there are at least two processes involved in gene expression that are strongly influenced by metabolism acetylation and methylation. Histone acetylation is regulated by availability of acetyl CoA produced in mitochondria, generally acetylation activates and promotes genes and deacetylation represses them.

Methylation generally decreases expression of certain genes, various things that interfere with mitochondrial metabolism increase methylation for example hypoxia and BPA (Nahar et al. 2015). Methylation and hypermethylation of various genes (NADH dehydrogenase, cytochrome oxidase and PGC-1A) involved in promoting metabolism is involved in obesity and diabetes (Barres and Zierath 2011).

It was believed that methylation represented a relatively permanent modification, with demethylation limited to relatively passive processes occurring during DNA replication and embryogenesis, however active demethylation has been found to occur quite commonly. Active demethylation is dependent on the availability of metabolites of the citric acid (Krebs/TCA) cycle (Meng et al. 2014).

Respiratory energy production has increased as evolution has advanced allowing for increasing cephalisation and intelligence, if an organism with an intense metabolic rate suddenly found its metabolism  lowered all the biological structure dependent on that energy production would degrade including the consciousness, gene expression would change, methylation would increase.

If maintaining our current state is dependent on generating a certain level of energy production then perhaps cultivating a higher level of energy production will help to make possible an increase in developmental complexity. Increased rates of DNA synthesis and nucleotide substitution occur in organisms with higher metabolic rates (Martin and Palumbi 1993). An advance to neo-human perhaps even post-mammalian life may be a real possibility.

The story goes that when Bodhidharma arrived at the Shaolin temple he found monks who were too weak to meditate successfully, so he developed a series of postures and movements linked to the breath (these eventually developed into Shaolin kung fu) for the monks to practice to assist in their cultivation. These exercises would have cultivated type 1 muscle fibres and increased the monks PGC-1A expression increasing their vitality.

The monks could then meditate meaningfully, meditation has been found to increase the gyrification (the convolutions and surface area) of the cortex of the brain (Luders et al. 2012). This increase in cortical gyrification seems likely to involve increased expression of HAR1 and Reelin.

It seems somewhat unlikely to be coincidence that yogic practices just happen to involve the activity of two highly significant human accelerated regions.


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Muscle, metabolism, mitochondria, and metamorphic mutation Magick

“Why should you study and practice Magick?

Because you can’t help doing it, and you had better do it well than badly.”

-Aleister Crowley 666

Tantravayanarasana (Peter Parker's pose).

Tantravayanarasana (Peter Parker’s pose). “With great power, comes great responsibility.”

Part 1: Posture and Prana

The use of static postures as exercises is common to both Hatha Yoga and systems such as Qigong and various internal martial arts such as Tai Chi Chuan, these postures are often recommended to be held for extreme lengths of time for example 3 hour headstands and stories of Internal Kung fu masters who would not accept a student unless they could hold a posture such as “embracing the tree” for 2 hours. To people familiar with only typical exercises involving repetitive gross movements, these static practices often seem odd, masochistic, pointless, or even insane. However if we think about the body in greater depth these practices might turn out to be wily and wise.

There are two main types of muscle fibre in the body, type 1 slow contracting fibres heavily reliant on oxidative metabolism, possessing high quantities of mitochondria (the cellular organelles responsible for energy production), these type 1 fibres possess a rich capillary network and are red in colour, these muscle fibres are those which must be active for extended periods of time, maintaining posture or engaged in continuous but hopefully not too strenuous activity. The type 2 fibres, of which there is a further variety of subtypes, are less reliant on oxidative metabolism, making greater use of glycolysis, a less efficient form of energy production that produces less ATP than oxidative metabolism and more lactic acid, they contain fewer mitochondria, these fibres are generally white in colour as they have less blood supply, these fibres contract quickly and powerfully and are used when bursts of explosive power are required. Muscle tissue exhibits a high degree of plasticity,  up regulation and down regulation of the different fibre types occurs in response to use and disuse. Nerve impulse patterns, neuromuscular activity, and mechanical loading play roles in the maintenance and transition of muscle fibre phenotypes. The type, intensity, and duration of changes in any of these factors, can cause muscle fibres to shift their phenotype to respond to the altered demands. Fibre transitions result from multiple changes in gene expression involving up and down regulation of genes involved in producing different myosin types in the fibre types (Pette 2001). After inactivity the slow red (type 1) fibres decrease leaving an increased proportion of fast white (type 2) fibres. Paraplegic subjects develop uniform fast fibre muscle composition within 6-12 months of injury (Polla et al. 2004). Both endurance and resistance exercise can cause the conversion of 2X fibres to 2A fibres, type 2A fibres are better supplied by capillaries and have more mitochondria and greater oxidative metabolism than 2X fibres but the 2A are not as metabolically active as type 1 fibres. From all the available studies it appears much more difficult to increase type 1 fibres than other fibre types, extreme endurance exercise can do it but I think that can be problematic. However I suspect that if exercise such as Yoga posture and qigong standing practice were to be studied it might be found that they increase type 1 fibres. In addition to the long holds used being likely to stimulate type 1 fibres, there are studies which show that stretching appears to signal the conversion of type 2 muscles into type 1 (Goldspink et al. 1991). The muscle in this study was stimulated while in a stretched position , this is similar to the kind of activity in many yoga asanas where muscle must be active while stretched, this is not an eccentric contraction (where a muscle stretches while bearing a load, eg. walking downhill) which can damage mitochondria, but isometric contraction while the muscle is already stretched. The muscle in this study grew rapidly as much as 30% in 4 days. Muscles deprived of stretch will not differentiate into type 1 (Goldspink et al.1992). The slow controlled movements used in Tai Chi and qigong involve rhythmic waves on contraction and subtle stretching and would be expected to stimulate type 1 slow red postural muscle development.

Patterns of activity can reshape the organism, type 1 fibres can become type 2 fibres if subjected to either disuse or if activity patterns change from continuous slower more controlled movement to rapid contraction, these changes involve a decrease in innervation, slow myosin is turned off when contraction speed increases and the fibres become innervated by only single motor neurons.

Physical activity is known to have a trophic effect on the brain, it seems likely that the increased innervation of type 1 fibres would mean that activities that maintain and cultivate these muscle fibre types should have an increased trophic effect on the brain, the more challenging balance and inverted postures of yoga seem especially likely to have such an effect, the slow controlled movements of Tai Chi should function similarly, as should dance, and multiple other activities climbing seems likely to cultivate type 1 fibres and have an increased trophic effect on the brain as the climber actively imagines routes up a rock face.

The postural muscles also seem likely to play a role in the organism’s energy level, in addition to containing more mitochondria than type 2 muscle fibres, type 1 fibres express more of an enzyme that converts T4 into the active thyroid hormone T3, type 2 iodothyronine deiodinase (Marsili et al. 2010). It seems possible that postural habits may be capable of signaling up or down regulated metabolism, if postural muscles are inactive this might lead to increased circulating T4, there is some evidence that increased T4 can suppress metabolism through conversion to reverse T3 suppressing mitochondrial respiration (Goumaz et al.1987).

Diabetics have reduced type 1 fibres and increased proportions of type 2 fibres (Oberbach et al. 2006). Cultivating type 1 fibres through exercise and lifestyle might be therapeutic.

The increased metabolic activity of type 1 fibres is also likely to contribute to softer and more fluid connective tissues, as the increased carbon dioxide, produced from oxidative metabolism, will interact with the amino groups of proteins and glycoproteins that make up the connective tissues altering the way these proteins interact with water leading to a more fluid and flexible body.

As people age they tend to experience muscle loss and become more prone to falls and consequent bone fractures, during aging blood flow and the capillary to fibre ratio decreases, promoting the development of the type 1 postural muscles would seem to be of importance in avoiding the increasing danger of medicalisation with age.

Increased activity of the postural muscles will support structural integrity of the body at multiple levels, blood flow efficiency will be increased, the increased innervation will also make body fat accumulation less likely as denervation can increase lipogenesis (Youngstrom and Bartness 1998).

Continual cultivation of perpetual poise discourages development of such sicknesses as hernias and haemorrhoids.

Part 2 Asana and Attitude

Some see Nature all Ridicule & Deformity, & by these I shall not regulate my proportions; & some scarce see Nature at all. But to the Eyes of the Man of Imagination, Nature is Imagination itself. As a man is, so he sees. As the Eye is formed, such are its Powers.”

-William Blake

In addition to effects on muscle phenotype posture has other subtler effects, different postures involve different patterns of nerve activity which will affect the endocrine organs, including the thyroid a master regulator of metabolism, conscious shifts in posture will change innervation patterns and endocrine function. A study examining the effects of posture on hormone function found that adopting an expansive posture for even a minute or two could lead to elevated testosterone and decreased cortisol (Carney et al. 2010). The same study found that individuals who adopted open expansive postures were more likely to engage in risky behaviour, individuals who adopted collapsed low power postures showed decreased testosterone and elevated cortisol and were more risk averse.

It seems likely that posture can affect every hormone produced, systems such as yoga and qigong all emphasise the importance of the spine, and seek to cultivate strong, flexible spines, they also emphasise keeping the spine straight during meditation, with yoga emphasising postures such as padmasana (lotus) and siddhasana (adepts/perfect) both of which encourage a very straight alignment of the spine, with the back of the neck kept long, this alignment seems likely to encourage production of the youth associated neurosteroids, pregnenolone, progesterone, and dhea. This sort of alignment is intensified during pranayama performed with mulabandha (contraction of the pelvic floor), uddiyana bandha (vacuuming the abdomen in and up under the rib cage), and jalandhara bandha (contraction of the throat with the chin dropping in towards the space between the collar bones).

Krishnamacharya applying jalandhara, uddiyanna, and mula bandhas while in mulabandhasana.

Krishnamacharya applying jalandhara, uddiyanna, and mula bandhas while in mulabandhasana.

Given these effects of posture on biology it should be possible to make therapeutic use of postural play to transform multiple challenges individuals are faced with, even conditions where it is believed an individual has encountered an impassable genetic wall in the developmental unfolding might be capable of change, Down’s syndrome, caused by an extra copy of chromosome 21 might seem like one of these impassable genetic walls, but this attitude seems inherently limiting. Individuals affected by Down’s syndrome generally show some common postural features, including a forward head posture and generally poor muscle tone, if affected individuals could be encouraged into new postural habits some change might be possible. The forward head posture likely alters blood and cerebrospinal fluid flow to the brain inhibiting its full development. Seeing the trophic effects of exercise on the brain as well as the trophic effects of the brain on tissues, there is clearly considerable inertia to overcome in this condition but change may be possible if skillful means are used to encourage new postural patterns, and other supportive therapies are included that focus on optimising metabolism.

Yogis say that organisms practice asana (posture) in the womb or egg to develop themselves.

Yogis say that organisms practice asana (posture) in the womb or egg to develop themselves.

Shifts in postural muscle use over generations seem likely to be a significant factor driving speciation, changes in environment would lead to shifts in how the organism interacts with its environment and moves through its environment. New patterns of muscle activity will change nerve activity reshaping an organism’s consciousness as it actively imagines new ways of relating to its environment.

Coyote carefully concentrates, cunningly crafting chaotic capers.

Coyote carefully concentrates, cunningly crafting chaotic capers.

Part 3: Diaphragmic Diabolism

Concentration is the root of all the higher abilities in man.”

Bruce Lee

The diaphragm is major postural muscle in humans and has great significance in preserving our highest functioning. The diaphragm is a uniquely mammalian structure, reptiles and amphibians have only a non-muscular membraneus septum separating the lungs from the digestive organs, or in some a pseudo diaphragm. Reptilian lungs have relatively coarse structure, larger air spaces and less surface area than mammalian lungs, amphibian lungs are simpler still, often little more than simple balloon structures, some amphibians lack lungs and breathe through their skin. Mammals have highly lobated alveolar lungs, with very large surface area and high diffusion capacity but low compliance, it is our muscular diaphragm which  enables them to function efficiently through the creation of negative pressure allowing for fine control of ventilation. The structure of our lungs and diaphragm is key to maintaining our intense metabolism. If these structures degrade then systemic degeneration is inevitable unless function can be restored, the organism will be forced to function at a lower energy level, one that is incapable of maintaining the complex structures we have developed over the course of our evolution.



Small mammals (such as shrews and mice) have high metabolisms, the fibre composition of their diaphragm is in some cases uniformly made up of type 1 slow red  oxidative muscle fibres, dense in mitochondria. Large mammals (such as cows) have a proportionally lower metabolism, their diaphragms contain a higher proportion of type 2 fast white glycolytic fibres, with fewer mitochondria.

Small mammals breathe more times per minute than large mammals, these breaths will involve more continual activity of the diaphragm, promoting type 1 slow red fibres. Large mammals breathe more slowly, but these movements are intermittent  and less isometric tension will be maintained through the diaphragm, promoting  type 2 fast white glycolytic fibres (Gautier and Padykula 1966).

Does the metabolic activity of the diaphragm reflect the overall metabolic intensity of the organism? A tendency seen in evolution appears to be a movement to generally finer muscle fibres, amphibians and reptiles tend to have thicker muscle fibres than birds and mammals, type 1 fibres are thinner than type 2 fibres, this suggests that as organisms evolve and raise their energy level they become more finely woven.

Cultivating the function of the diaphragm might be capable of raising our energy level, I have seen a few claims that the diaphragm cannot be exercised but I think the individuals who made these claims have not thought them through sufficiently. In addition to its function in respiration the diaphragm is also a postural muscle one that plays a key role in maintaining our characteristically upright posture, stabilising our body during a range of movements (Hodges et al. 1997). Activities that require complex postural stabilisation; dance, hand balancing and some of the more demanding postures and transitions of yoga should all strengthen and tone the diaphragm.

The traditional pranayama practices of Hatha Yoga will also train and cultivate the diaphragm, the practice of uddiyana bandha combined with kumbhaka (breath retention), will both stretch the diaphragm and tone it through isometric contraction, both of which cultivate type 1 muscle fibres. The type of breathing emphasised in some qigong systems, a very fine, long slow, and super subtle breath, without retentions should also work similarly.

If there are activities that  can cultivate the diaphragm there are likely activities that do the opposite generally unconscious postural habits might lead to the degeneration of some of the diaphragm’s function, if it is not needed then tissue tends to degenerate, fear furniture.

While extreme endurance activity tends to promote type 1 muscle fibres in most skeletal muscles, I think in the diaphragm it might have the opposite effect. Extreme endurance athletes have been found to show increased rates of asthma (Helenius et al. 1997). This might be a result of the increased oxygen demand during exercise leading to increased ventillaton, and larger coarser movements of the diaphragm, resulting in the phenotype of the diaphragm muscle fibres shifting away from the slow red type 1 towards increased fast white type 2 fibres, this would also result in decreased innervation to the diaphragm making it difficult to control breathing at rest, promoting hyperventilation, carbon dioxide loss, decreasing the Bohr effect and so decreasing oxygenation of tissues at rest. If people insist on that sort of endurance exercise then it might be useful to also practice breath control at rest to promote type 1 muscle fibres as well as being attentive to breathing during exercise.

Increased type 1 fibres are found in chronic obstructive pulmonary disease (COPD), however other pathological alterations to the respiratory system have also occured here, the lungs become inflamed, functional surface decreases, the lungs lose surface area, airspaces enlarge, the lungs swell and the diaphragm becomes chronically shortened, the muscle fibres lose sarcomeres, now the diaphragm can only make small rapid movements, and other muscles of the chest heave in an attempt to overcome the lost function.

Another activity that will lead to a degeneration of diaphragm function is breathing exercise performed badly due to misunderstandings, I have met a few people who seem to have made their breathing habits worse through breathing exercises, when you practice notice what is happening. People often talk about practicing deep breathing, they mean exchanging large volumes of air massively altering the internal atmosphere of the lungs, carbon dioxide and water vapour are lost, and the highly sensitive membranes of the lungs become damaged and inflamed losing their efficiency. Often these individuals will have been told pranayama is good because it increases the elimination of useless waste products of metabolism such as carbon dioxide, a completely mistaken idea. Mouth breathing is likely the worst breathing habit, the enlarged airway means the diaphragm will not be called to work  effectively, type 1 slow red fibres will be down regulated, encouraging a less innervated diaphragm, decreasing control of breathing,  causing degeneration and the lowering of an organism’s energy level.

When people ask me about breathing I usually recommend Buteyko, as the importance of carbon dioxide is understood, and the basic reduced breathing exercise of Buteyko will develop the diaphragm to some extent, however I suspect that more complete diaphragmatic development will occur through sensitively applied traditional yoga breathing methods, that incorporate bandhas and kumbhakas, however I may be mistaken (I’m still learning).

PsychicSine Waves. Psyche, from the greek psychein-to breathe. a.rapid coarse breathing, will lead to carbon dioxide loss and decreased Bohr effect. b.

PsychicSine Waves.
Psyche, from the greek psychein-to breathe.
a.rapid coarse breathing, will lead to carbon dioxide loss and decreased Bohr effect.
b.”normal” breathing.
c. coarse deep breathing will lead to carbon dioxide loss and decreased Bohr effect.
d. reduced breathing (Buteyko style).
e. yogic breathing, slow deep with breath retentions.
f. smooth, slow, deep breathing.
c. e. and f. will all move the diaphragm through a wide movement range.
e. andf. will cultivate control and development of the diaphragm. c.may over time lead to decreased control of the diaphragm with less innervation.
These are approximate representations, many more breath variations are possible. Yes I know some of the above are not really sine waves.

The way the diaphragm is used during breathing can effect blood flow dynamics, the use of uddiyanna bandha, seems to increase venous return to the heart, and likely stretches the heart causing the release of the heart hormones (natriuretic peptides) that further raise the organism’s energy level.

A safe focus for breath control is to seek to make your breathing ever finer and subtler, ideally at rest it should be imperceptible, if you were to place a hand directly beneath your nose the breath should not be felt, it should be silent, and the muscular movements should be so slow and subtle that only a sharp eye would notice. Breathe through your nose, when you mouth breathe you enlarge your airways allowing for large shifts in the internal atmosphere of the lungs, losing carbon dioxide and water vapour. The reduced breathing exercises of Buteyko are safe for most people focused on improving health, though I think some practices that make use of larger diaphragmatic movements would complement the practice. The simple “ujayi” breath used in Astanga Vinyasa is also useful, the increased awareness of the breath caused by the gentle contraction at the base of the throat and the resulting Darth Vader type sound bring increased awareness, during more challenging asana and vinyasa the breath will be louder. Sensitivity to the breath can be increased using ear plugs or inactive headphones, allowing you to hear the breath as it travels through the nasal turbinates and refine it further.


Carney DR, Cuddy AJC, and Yapp AJ, (2010), Power posing: brief non-verbal displays affect neuroendocrine levels and risk levels, Psychological Science.

Gautier GF, and Padykula HA, (1966), Cytological studies of fiber types in skeletal muscle, Journal of Cell Biology, 28, pp. 333-354.

Goldspink G, Scutt A, Martindale J, Jaenicke T, Turray L, Gerlach GF, (1991), Stretch and force generation induce rapid hypertrophy and myosin isoform gene switching in adult skeletal muscle, Biochemical Society Transactions, 19(2), pp. 368-373).

Goldspink G, Scutt A, Loughna PT, Wells DJ, Jaenicke T, Gerlach GF, (1992), Gene expression in skeletal muscle in response to stretch and force generation, AJP-Regu Physiol, 262(3), pp.356-363.

Goumaz MO, Kaiser CA, Burger AG, (1987), Brain cortex reverse triiodothyronie (rT3) and triiodothyronine (T3) concentrations under steady state infusions of thyroxine and rT3, Endocrinology, 120(4), pp. 1590-1596.

Helenius IJ, Tikkanen HO, Haahtela T, (1997), Association between type of training and risk of asthma in elite athletes, Thorax, 52, pp.157-160.

Hodges PW, Butler JE, McKenzie DK, Gandevia SC, (1997), Contraction of the human diaphragm during rapid postural adjustments, Journal of Physiology, 505(2), pp. 539-548.

Marsili A, Ramadan W, Harney JW, Mulcahey M, Castroneves LA, Goemann IM, Wajner SM, Huang SA, Zavacki AM, Maia AL, Dentice M, Salvatore D, Silva JE, Larsen PR, (2010), Type 2 iodothyronine deiodinase levels are higher slow-twitch than fast-twitch mouse skeletal muscle and are increased in hypothyroidism, Endocrinology, 151(12), pp. 5952-5960.

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Heart Hormones, Inversions, and Immortality

“Marshalling the information needed to optimize our own development runs counter to the program of our technical-scientific culture, which prefers to believe that degeneration is programmed, while emergent evolution is unforeseeable. But, if an optimization project is presented as a way to forestall the “programmed degeneration,” it might succeed in becoming part of the culture.”

-Ray Peat


alpāhāro yadi bhavedaghnirdahati tat-kṣhaṇāt |
adhaḥ-śirāśchordhva-pādaḥ kṣhaṇaṃ syātprathame dine || 81 ||

kṣhaṇāchcha kiṃchidadhikamabhyasechcha dine dine |
valitaṃ palitaṃ chaiva ṣhaṇmāsordhvaṃ na dṝśyate |
yāma-mātraṃ tu yo nityamabhyasetsa tu kālajit || 82 ||


“If he stints his diet, the fire quickly consumes [the body]. On the first day he should stand for a moment on his head, with his feet above.

After six months, the wrinkles and grey hair are not seen. He who practises it daily, for one yama (3 hours), conquers death.”


-from the Hatha Yoga Pradipika by Swatmarama (in reference to the Headstand / Viparita karani Mudra).

Dharma Mittra in headstand

Dharma Mittra in headstand

            So yet again those degenerate Hatha Yogis obsessed by the body and materiality are making outlandish and absurdly inflated claims for their circus tricks, before we saw how they claimed pranayama can cure all disease, now they expect prudent and reasonable human beings to believe that standing on your head will make you immortal, whatever next, yoga can turn you into an Elf?

If you believe in a biology crafted out of the random chance errors of a clockwork horror story “red in tooth and claw” then the claims made by some Hatha Yogis as well as other devils might appear insane, however taking another perspective on biology the picture is very different. In an organismic model where the liquid crystalline structure is generated and supported by the controlled coherent fire of the respiratory whirlwind, where processes are interconnected across all scales, then it might be possible to make creative use of local effects to generate systemic changes which further modify local processes. A range of relatively simple techniques for generating creative constructive adaptation that is capable of overcoming the organism’s assimilated inertia might make themselves available.

I believe that Hatha Yoga is an art that has discovered such creative techniques, and increasingly the evidence exists to make this case.

The Natriuretic peptides are a class of hormones secreted by the heart, while they are named for the observation that they can increase the urinary elimination of sodium they have a range of much more interesting effects. A major stimulus for their release is the stretching of the chambers (atria and ventricles) of the heart (Espiner et al.1995).

There is some evidence that inversions (turning upside down) cause an increased stretch in the chambers of the heart, as might be expected due to increased venous return of blood to the heart. A study examining the circulatory effects of the head down position showed increases in stroke volume, and cardiac output and a decrease in pulse rate (Wilkins et al. 1950). A study looking specifically at the yoga postures Sirshasana (headstand) and Sarvangasana (shoulderstand) found a significant increase in early left ventricle filling, a shortening of the isovolumetric relaxation time and an increase in heart rate (Minvaleev et al. 1995). If inversions are stretching the hearts chambers then they should be stimulating the release of the Natriuretic peptides, as far as I am aware no studies have looked at this possibility so there is some speculation here.

The Cardiac natriuretic peptides include six hormones stored as three separate prohormones, Atrial Natriuretic peptide (ANP), B-type natriuretic peptide (BNP), and C-type natriuretic peptide (CNP). ANP contains: long-acting natriuretic peptide (LANP), vessel dilator, kaliuretic peptide, and ANP (Vesely 2006).

The Natriuretic peptides have a wide range of effects, they have been shown to be anti-inflammatory, ANP reduced the secretion of inflammatory mediators produced in response to bacterial endotoxin /lipopolysaccharide (Kiemer and Vollmar 2001). Both ANP and CNP reduced the expression of COX-2 and prostaglandin E2 (PGE2) in response to lipolysaccharide (Kiemer et al. 2001). Anti-fibrotic , mice lacking BNP develop multiple fibrotic lesions (Tamura et al. 2000), BNP also appears to inhibit the profibrotic TGF-ß and increased collagen 1 and fibronectin proteins (Kapoun et al. 2004). ANP appears to have a tissue stabilising effect that prevents leakiness, ANP inhibited VEGF (vascular endothelial growth factor), protected the integrity of the blood-retinal-barrier of rats, ANP also significantly reduced the damage done by laser injury (being a lab rat sucks) ( Lara-Castillo et al. 2009). ANP has been found to defend the endothelial barrier from histamine induced permeability (Fürst et al. 2008).

These cardiac peptides appear to have some significant anti-cancer activity, in 24 hours, Vessel dilator, LANP, Kaliuretic peptide and ANP decreased the number of human pancreatic adenocarcinoma cells in culture by 65%, 47%, 37% and 34% respectively. Vessel dilator completely stopped the growth of human pancreatic adenocarcinomas in mice, further decreasing the size of even palpable large tumors, after 1 week vessel dilator decreased the size by 49%, LANP by 28%, and kaliuretic by 11%, in placebo treated mice the tumor had increased in size by 20 fold.

These hormones also decreased the number of breast adenocarcinoma cells by 60%(vessel dilator), 31%(LANP), 27% (kaliuretic), 40% (ANP). Other cancers; decreased cell numbers of small cell lung cancer, squamous lung cancers, and malignant tumors of the heart (Vesely 2005).

A study examining the effects of CNP on proliferating smooth muscle cells found that CNP induced growth inhibition and promoted re-differentiation into highly differentiated smooth muscle cells rather than the less differentiated proliferative phase, CNP improved healing accelerating re-endotheliazation preventing neointima formation (Doi et al. 2001).

The cardiac peptides also decrease some hormones associated with stress, perhaps most interestingly prolactin (Samson et al. 1998), but also ACTH which contributes to cortisol (a catabolic hormone released by stress) release (Fink et al. 1991). Swatmarama states that headstand can reverse greying of hair, and prolactin has been implicated in hair loss (Foitzik et al. 2006).

These effects of the cardiac peptides, anti-inflammatory, tissue stabilising and anti-cancer suggest that it might be appropriate to view these hormones as in some sense bioenergetic kosmotropes that increase the coherence of the organism, as Energy and structure are interdependent, at every level”* then substances that increase structural coherence should in some way increase energy as an increase in structure should allow for an increase in energy flow which would in-turn allow for structural complexification.

ANP and BNP have been found to induce mitochondriogenesis (making new mitochondria) , and to increase “uncoupled” respiration, that is to increase respiration while producing less ATP, instead increasing heat production, this might seem wasteful but it appears protective. White adipose tissue appeared to become more like brown fat tissue, brown fat contains more mitochondria than white, and is especially abundant in infants, increased levels and activity of brown fat has been linked to resistance to metabolic diseases such as diabetes and obesity (Bordicchia et al. 2012). A separate study found that BNP protected against diet induced obesity and insulin resistance and increased muscle mitochondrial content (Miyashita et al. 2009).

With the prevalence of mechanical thinking in biology some people might think that increased metabolism means increased wear and tear on the lumbering bio-robot that is piloted by their consciousness (probably an illusion generated by those selfish genes), if the organism is generated by the metabolic flow of energy, the increased metabolism would be expected to result in increased renewal and rejuvenation. In mice individuals with higher metabolisms and greater mitochondrial uncoupling lived longer (Speakman et al. 2004). Somewhat obviously disuse of a tissue results in atrophy, and mitochondria demonstrate increased reactive oxygen species (ROS) and decreased respiratory enzymes.

Given the evidence for the role of intensified metabolism in evolutionary progress it seems especially difficult to take seriously any attempt to market torpor as a preferable biological state. Mammals have more intense metabolisms than reptiles from 2 to 5 times more, possibly even greater in the case of some humans, mammals also have greater thyroid activity than reptiles (Hulbert and Else 1981). This increased metabolic activity in mammals has required adaptative complexification of the cardiopulmonary system to support it, this is one of the clearest examples of aromorphosis (a raising of the shape making a higher level of function available), an increased metabolism and increased oxygen use required a development and complexification of the Heart and circulatory system, the generation of a four chambered heart made it possible to operate at a higher, more generous energy level. Generally, fish have a two chambered heart, amphibians three chambers, two atria and one ventricle, from here things get a little more complicated as many species of reptile have varying degrees of ventricular septation with a ventricle that has not quite divided into two separate chambers, meaning that blood flow can complexify and increase in efficiency but not to the degree of birds, and mammals which have four chambered hearts (Jensen et al. 2013). To complicate things crocodilians have four chambered hearts and lungs which are similar to bird lungs.

Morphology of the heart of various animals (Jensen et al. 2013)

Morphology of the heart of various animals (Jensen et al. 2013)

I think the case can be made that the cardiac peptides are sorts of morphogen, substances that are involved in biological structure generation and regulation, which would be dependent on available energy, decreased energy tends to result in a sort of organismic shrinking, and poor circulation, the effects of an energy surplus can be felt after a large meal, a sort of pleasant expansive, metabolic flush, an increase in circulation, pranayama also can produce such an effect, which should result in increased stretch being experienced in the heart. It seems reasonable to suggest the heart as sort of morphogenic regulator.

These Cardiac peptides are higher in the foetal circulation than adults, and the foetal heart expresses higher levels of these hormones than the adult heart. Peaks of ANP and BNP during gestation coincide with significant moments during cardiac morphogenesis (Cameron and Ellmers 2003).

These peptides also appear to play a role in bone remodelling, CNP is a potent stimulator of osteoclast activity demonstrating a role in bone remodelling (Holliday et al. 1995). CNP also stimulates chondrocyte proliferation, cartilage matrix production and long bone growth in foetal rats (Mericq et al. 2000).

If these cardiac peptides are sorts of morphogen then they might be expected to be increased by other signs of increased energy availability, such as increased thyroid activity and steroid hormones this appears to be the case, thyroid hormones T3 and T4 (T3 being more active) and testosterone dose dependently stimulated ANP (Matsubara et al. 1987). ANP at least in some studies stimulates testosterone production (Pereira et al. 2008), I think this points to the possibility of some self-intensifying positive feedback loops at least when energy is available to nurture them. Life appears to desire to be ever more.

“Energy is the only Life…”

*apologies to Ray Peat for totally overusing this quote (the “Energy and structure…”one), and also for the neural architecture I stole, you can’t have it back, and anyway I fear it’s been irreversibly warped by my own context.


Bordicchia M, Liu D, Amri E-Z, Ailhaud G, Dessi-Fulgheri P, Zhang C, Noboyuki T, Sarzani R, Collins S, (2012), Cardiac natriuretic peptides act via p38 MAPK to induce the brown fat thermogenic program in mouse and human adipocytes, J Clin Invest, 122(3), pp 1022-1036.

Cameron VA, and Ellmers LJ, (2003), Minireview: natriuretic peptides during development of the fetal heart and circulation, Endocrinology, 144(6).

Doi K, Ikeda T, Itoh H, Ueyama K, Hosoda K, Ogawa Y, Yamashita J, Chun T-H, Inoue M, Masatsugu K, Sawada N, Fukunaga Y, Saito T, Sone M, Yamahara K, Kook H, Komeda M, Ueda M, Nakao K, (2001), C-type natriuretic peptide induces redifferentiation of vascular smooth muscle cells with accelerated reendotheliazation, Arteriosclerosis, Thrombosis, and Vascular Biology, 21, pp. 930-936.

Espiner EA, Richards AM, Yandle TG, Nicholls MG, (1995), Natriuretic hormones, Endocrinology and Metabolism Clinics of North America, 24(3), pp. 481-509.

Fink G, Dow RC, Casley D, Johnston CI, Lim AT, Copolov DL, Bennie J, Carroll S, Dick H, (1991), Atrial natriuretic peptide is a physiological inhibitor of ACTH release: evidence from immunoneutralization in vivo, J Endocrinol, 131, pp. 9-12.

Foitzik K, Krause K, Conrad F, Nakamura M, Funk W, Paus R, (2006), Human scalp hair follicles are both a target and a source of prolactin which serves as an autocrine and/or paracrine promoter of apoptosis-driven hair follicle regression, American Journal of Pathology, 168(3), pp. 748-756.

FürstR, Bubik MF, Bihari P, Mayer BA, Khandoga AG, Hoffman F, Rehberg M, Krombach F, Zahler S, and Vollmar AM, (2008), Atrial natriuretic peptide protects against histamine-induced endothelial barrier dysfunction in vivo, Molecular Pharmacology, 74(1), pp. 1-8).

Holliday LS, Dead AD, Greenwald JE, Gluck SL, (1995), C-type natriuretic peptide increases bone resorption in 1,25-dihydroxyvitamin D3– stimulated mouse bone marrow cultures, Journal of Biological Chemistry, 270, pp. 18983-18989.

Hulbert AJ, and Else PL, (1981), Comparison of the “mammal machine” and the “reptile machine”: energy use and thyroid activity, AJP- Regu Physiol, 241(5), pp. 350-356.

Jensen B, Wang T, Christoffels VM, Moorman AFM, (2013), Evolution and development of the building plan of the vertebrate heart, BBA- Molecular Cell Research, 1833(4), pp.783-794.

Kapoun AM, Liang F, O’Young G, Damm DL, Quon D, White RT, Munson K, Lam A, Schreiner GF, Protter AA, (2000), B-type natriuretic peptide exerts broad functional opposition to transforming growth factor-ß in primary human cardiac fibroblasts, Circulation Research, 94, pp. 453-461.

Kiemer AK, and Vollmar AM, (2001), The atrial natriuretic peptide regulates the production of inflammatory mediators in macrophages, Ann Rheum Dis, 60, pp. 68-70.

Kiemer AK, Lehner MD, Hartung T, and Vollmar AM, (2001), Inhibition of Cycloxygenase-2 by natriuretic peptides, Endocrinology, 143(3).

Lara-Castillo N, Zandi S, Nakao S, Ito Y, Noda K, She H, Frimmel S, Ablonczy Z, Hafezi-Moghadam A, (2009), Atrial natriuretic peptide reduces vascular leakage and choroidal neovascularisation, Am J Pathol, 175(6), pp. 2343-2350.

Matsubara H, Hirata Y, Yoshimi H, Takata S, Takagi Y, Iida T, Yamane Y, Umeda Y, Nishikawa M, Inada M, (1987), Effects of steroid and thyroid on synthesis of atrial natriuretic peptide by cultured atrial myocytes of rat, Biochemical and Biophysical Research Communications, 145(1), pp. 336-343.

Mericq V, Uyeda JA, Barnes KM, de Luca F, and Baron J, (2000), Regulation of fetal rat bone growth by C-type natriuretic peptide and cGMP, Pediatric Research, 47, pp. 189-193.

Minvaleev RS, Kuznetsov AA, Nozdrachev AD, Lavinskii YK, (1995), Left ventricle filling in sirsasana and sarvangasana yogic postures, St Petersberg State University.

Miyashita K, Itoh H, Tsujimoto H, Tamura N, Fukunaga Y, Sone M, Yamahara K, Taura D, Inuzuka M, Sonoyama T, Nakao, K, (2009), Natriuretic peptides / cGMP/ cGMP-dependent protein kinase cascades promote muscle mitochondrial biogenesis and prevent obesity, Diabetes, 58(12),pp. 2880-2892.

Pereira VM, Costa APR, Rosa-e-Silva AAM, Viera MAR, dos Reis AM, (2008), Regulation of Steroidgenesis by atrial natriuretic peptide (ANP) in the rat testis: differential involvement of GC-A and C receptors, Peptides, 29(11), pp. 2024-2032.

Samson WK, Bianchi R, Mogg R, (1988), Evidence for a dopaminergic mechanism for the prolactin inhibitory effect of Atrial Natriuretic factor, Neuroendocrinology, 47, pp. 268-271.

Speakman JR, Talbot DA, Selman C, Snart S, McLaren JS, Redman P, Krol E, Jackson DM, MS Johnson, Brand MD, (2004), Uncoupled and surviving:individual mice with high metabolism have greater mitochondrial uncoupling and live longer, Aging Cell 3(3), pp. 87-95.

Tamura N, Ogawa Y, Chusho H, Nakamura K, Nakao K, Suda M, Kasahara M, Hashimoto R, Katsuura G, Mukoyama M, Itoh H, Saito Y, Issei T, Hiroki O, Katsuki M, Nakao K, (2000), Cardiac fibrosis in mice lacking brain natriuretic peptide, PNAS, 97(8),pp. 4239-4244.

Veseley D, (2005), Atrial natriuretic peptides: anticancer agents, Journal of Investigative Medicine, 53(7), pp. 360-365.

Veseley D, (2006), Which of the cardiac natriuretic peptides is most effective for the treatment of congestive heart failure, renal failure, and cancer? Clinical and Experimental Pharmacology and Physiology, 33(3), pp. 169-176.

Wilkins RW, Bradley SE Friedland CK, (1950), The acute circulatory effects of the head-down position (negative G) in normal man, with a note on some measures designed to relieve cranial congestion in this position, J Clin Invest, 29(7), pp.940-949.

The Starchild Skull: a third perspective, aromorphic evolution?

“He whose face gives no light shall never become a star.”

-William Blake

“Every man and every woman is a star.”

-Aleister Crowley

“The infant represents our evolutionary future.”

-Ray Peat 


Aromorphosis: noun; plural aromorphoses; from Greek airein, to raise; morphosis, shaping.  An advancement in the organization of an organism, without a marked increase in specialisation; an aromorph.

“a morphological and physiological process, one of the main trends in the biological progress of living organisms whereby their organization becomes increasingly complicated in the course of evolution. The term was introduced by A. N. Severtsov, who used the word “aromorphosis” to refer to the most general adaptive changes in organization and functions. Aromorphosis is usually accompanied by an increase in the intensity of the life processes of animals and in the variety of their manifestations (differentiation)…. Aromorphosis enables qualitative jumps that raise the level of organization of a species…. As an example of aromorphosis in the evolution of higher vertebrates Severtsov cites the qualitative jump in the transition from reptilian ancestors to mammals. The four-chambered heart, the alveolar structure of the lungs, diaphragmatic breathing, and other factors raised the level of metabolism in mammals and increased their ability to adapt to changes in living conditions. Bearing young in the mother’s uterus and feeding them milk extended their chances of survival.”

from The Great Soviet Encyclopedia (1979).


The Starchild skull is a strange skull that was found in Mexico, somewhere between the region of the Sierra Madre Occidental mountain range (elevation: 10,863ft / 3,311 m), and about 100 miles southwest of Chihuahua, the skull appears to be around 900 years old according to radiocarbon dating. The skull exhibits a number of very unusual features leading to claims that it is either alien or a human-alien hybrid, the most notable proponent of the alien/ alien-human hybrid explanation was the late Lloyd Pye, on the other hand the “sceptics” claim the skull is simply a deformed human skull, one that admittedly exhibits a range of unusual features. I’m not convinced either of these two positions is true and would like to suggest a third tentative🙂 possibility.

First the unusual features of the skull:


The volume of the interior of the skull is 1,600 cubic cm, 200cm3 larger than the average adult’s and 400cm3 larger than an adult of equivalent size.


The orbits of the eyes are oval and unusually shallow.

It appears the skull would have had relatively small cheek bones and small muscles for chewing food as these muscles pass through the zygomatic arches.


The skull lacks frontal sinuses.

The bone is unusually thin, but also appears to be highly durable, exceptionally hard, Lloyd Pye has claimed that the bone was incredibly difficult to cut through and is woven through by odd fibres, yet to be identified.

A mineral analysis of the bone shows significant differences to typical human bone, most notably containing an unusually high amount of carbon and oxygen (carbon dioxide?).

mineral analysis

mineral analysis

Genetic material recovered from the skull appears unusual, mitochondrial DNA from the starchild skull differs from human, generally the maximum number of mtDNA variations between humans is 120. The Starchild Skull has between 800-1,000 differences.

Nuclear DNA, some of the starchild’s nuclear DNA may be different from anything previously found on earth, including a fragment several thousand nucleotides long that could not be matched to any recorded DNA.

There are some issues with the interpretation and presentation of results of genetic testing by the Starchild Project, early tests appeared to show that standard X and Y chromosomes were present, suggesting that the child was a human male or at least had human parents. Mitochondrial DNA also appeared to belong to haplogroup C (a Native American group).

I don’t think the possibly significant genetic differences require extra-terrestrials to explain, given the evidence for non-random directed genetic mutation, it seems possible that a biology that is liquid crystalline and energetically coherent across multiple domains would allow for sudden meaningful and significant adaptive evolutionary jumps especially when conscious organismic intelligence is recognised as fundamental to and inseparable from biology. Organismic bioenergetic coherence would allow for seemingly vast evolutionary jumps with the new organism differing significantly and meaningfully at the genetic level from the parent organism.

The early results also strongly suggest the skull at least has a connection to earth humans.

What I would like to suggest is that the skull is neither deformed nor alien, instead it may be neo/meta-human, an evolutionary stride forwards.


So why do I think this might be the case? Well the skull and some of the reconstructions based on it appear remarkably neotenous, that is it preserves very youthful features, large brain size, large, eyes, relatively small face in comparison to the head size, for more on neoteny as an evolutionary tendency see:

Chapter 4 of Ray Peat’s Generative Energy


Ontogeny anticipates phylogeny: Evolution, meditation, and the brain.



I think the mineral analysis is interesting, if carbon dioxide is as biologically significant as I suspect, acting in some sense as a sort of electrical doping agent increasing the conductivity of proteins, it might be expected that a more evolved and energetic organism might show signs of exposure to higher levels of carbon dioxide.

For more on CO2 see:

Pranayama, Carbon Dioxide, Mitochondria, Coherent Energy Flow, Regeneration and Individuation


Rainbow worms, Electrobiology, Carbon Dioxide and the Streaming Auto Evolving Life Process

As well as Ray Peat’s articles and the Biology of Carbon dioxide video (see resources).

I think some of the unusual qualities of the bone might be explainable by increased trophic activity of the nerves, resulting in a more qualitatively developed bone as a result of increased quality of innervation, denervation of bone results in osteoporotic bone, so it does not seem unreasonable that increased nerve energy might result in a developmental advance in bone quality.

hydrocephalic skull

hydrocephalic skull

I’m not convinced by the explanation that the skull is of cradleboarded hydrocephalic infant, or a child with progeria, the morphology of the skull while unusual appears coherent and the unusual qualities of the bone, if Lloyd Pye has reported them accurately, seem incompatible with either hydrocephalus or progeria. In progeria bones show hypoplasia and dysplasia, yet the starchild bone is reported to be super-humanly tough.

I don’t think it’s necessary to bring extra-terrestrials into the picture to explain the starchild skull, other factors that might be involved include the altitude, leading to increased carbon dioxide retention on the part of both the child and mother, possible yogic / meditative / spiritual practice on the part of the mother resulting in an optimized uterine environment for the developing organism. If the skull is 900 years old this would place it within the Medieval warm period which lasted from AD 950 – 1250, in Europe this was a perid of abundant food as result of the warmer climate and milder winters, this abundance of food and more hospitable climate may have contributed to developments in art and culture that resulted in Gothic architecture, it is possible that these more nurturing conditions allowed for the aromorphic evolution seen in the Starchild skull. Other various and unknown reasons might also be involved, likely requiring a highly permissive environment free from the usual distorting cultural stressors a developing child would encounter, allowing for the child to devote its conscious energies to the realization and expansion of its developmental potentials, allowing for autopoietic evolution.

The suggestion that the starchild’s differences are a result of an autopoietic evolution might seem strange even impossible, but only if you believe in a stupid mechanical model of evolutionary change that depends on random mutations selected out by a blind mechanism “red in tooth and claw”, if it is recognized that evolution is a living organic participatory process that intimately involves conscious intelligence, then the suggestion that the starchild skull might be the result of a conscious organic probing into a new potential biopsychic state seems at least to me natural, and if this sort of evolution is possible for one then it must be possible for others.

Further Reading


A Bone to Pick with the Starchild Skull

The Starchild Project


The child’s toys and the old man’s reasons are the fruits of the two seasons.

“Once we accept that knowledge is tentative, and that we are probably going to improve our knowledge in important ways when we learn more about the world, we are less likely to reject new information that conflicts with our present ideas. The attitude of expectancy will allow us to apply insights gained at one level of generality to other levels. No particular kind of knowledge will have such authority that it will automatically exclude certain possibilities in another field of knowledge.”

Ray Peat


I don’t think enough emphasis can be placed on the quote above from Ray, as we learn and discover more experience deepens and old models whilst accurate in at least some respects may need to be re-evaluated in reference to larger perspectives as they are experienced, attachments to old descriptions and interpretive frameworks may acts as blinders and binders of more vital perspectives that may be immediately available to direct experience if only the mind forged manacles can be cast off.


“When you believe that you have adequate, expert knowledge, a passive, logical, deductive form of mental activity seems appropriate. Deduction always goes from a higher level of generality to a lower level of generality. Mental passivity therefore is likely to be associated with the belief that we have the decisive knowledge already stored in memory. If we believe that we create higher degrees of generality, as appropriate solutions to novel problems, then we are committed to an active mental life. Perception, combined with the discovery and invention of new patterns in the world, will be actively oriented toward the future, while the deductive, merely analytical, manner of thought will be tied to the past.”

Ray Peat


Remaining open to new perspectives encourages a youthful flexible mind, one that experiences the world intimately with a continual sense of wonder.

As we develop our world view must develop with us if our world view remains static it is likely that our possible growth and development is being inhibited.


The eagle never lost so much time, as when he submitted to learn of the crow.”


“As the true method of knowledge is experiment, the true faculty of knowing must be the faculty which experiences.”



“The ancient Poets animated all sensible objects with Gods or Geniuses, calling them by the names and adorning them with the properties of woods, rivers, mountains, lakes, cities, nations, and whatever their enlarged & numerous senses could percieve.
And particularly they studied the genius of each city & country, placing it under its mental deity;
Till a system was formed, which some took advantage of & enslav’d the vulgar by attempting to realize or abstract the mental deities from their objects: thus began Priesthood;
Choosing forms of worship from poetic tales.
And at length they pronounc’d that the Gods had order’d such things.
Thus men forgot that All deities reside in the human breast.”