Acupuncture & Chinese Medicine ● Longevity Nutrition

literary biohacking

In the temperate zones of the Earth, late summer into autumn has been a time of celebration in many cultures. This is the time when all creatures breathe a sigh of relief as the hard work of growth slows. The cooler air transforms summer’s searing rays of sunshine into loving, golden warmth. Pregnant with sugar, fruits of flowering plants hang heavy from the branches and dapple the landscape in a mosaic of reds, blues and purples from anthocyanins and carotenoids. On the ground, combinations of lutein and zeaxanthin color the winter squashes of the Cucurbita family with the same oranges and yellows that are revealed as chlorophyll relinquishes its dominion over the foliage.

Colorful pigments that once acted as a beacon for pollinators in an array of colors and hormones[1] assume a new form that will serve as this year’s bridge of survival for numerous species of birds and mammals, including humans.

Over these precious few weeks, concentrated glucose and fructose flow in like the ocean tide. With them, the stomach’s master hormones of appetite flip flop. Ghrelin’s waxing and leptin’s waning[2] impose an ever-rising voracity of appetite that has driven successful survival of species over hundreds of millions of years. Inside the sweet goodness lurks even more treasures. Fresh omega-six oils from seeds and grains give a fresh boost to dwindling eicosanoids that are crucial for cell-to-cell communication. Vitamin E, selenium[3], vitamin C and phytonutrients stand like a levy to ensure the rising tide of inflammation doesn’t breach its banks.

In Traditional Chinese Medicine Theory, this time of year was considered the fifth season associated with the Earth element.  Warmth, sunshine, water and Earth have been magically transformed by a billion tiny seeds into a form that passes life’s nourishment unto us.   In the Jewish tradition, this season beckons the new year known as Rosh Hashanah.

“Blessed are you, sovereign of the Universe who brings forth bread to the Earth…who has kept us in life, has sustained us and brought us to this season.” Torah

Lurking deep within the cell, all the way down to the nuclear membrane, a sugar-laden surge of insulin nudges a sleeping Goddess from her torpor. 2.1 billion years ago[4],[5] some of the earliest fungi birthed this goddess and time kindly bequeathed her unto humans. In science she is known as SREBP or sterol regulatory elemental binding proteins. She is the one who, as if by magic, signals that transformation of sugar into a form that can be stored for later use as triglycerides[6] and fat[7].  Without her, most animals in the temperate and arctic zones are unlikely to survive even one winter.

Because of SREBP’s, every cell can make its own LDL cholesterol for membrane repair and vitamin D synthesis. However, without a way to supply basic antioxidants to the cell, LDL quickly oxidizes. This transformation from Dr. Jeckel to Mr. Hide damages everything it touches[8] and is considered to be one of the driving forces of atherosclerosis7. In order to protect her inner world and ensure a constant supply of antioxidants, SREBP must ask for a little help from one of her cousins in the liver, SREBP-1. While most of the cells of the body settle for glucose as an energy source, the liver engages in a more refined taste for fructose. In fact, liver cells are the only ones that can use fructose and its effects are incendiary. Fructose drives rapid production of LDL cholesterol, fats and inflammation in the liver[9],[10]. This preference for fructose acts as a supply chain for the trillions of cells’ insatiable need for antioxidants during times like these. But without SREBP, these antioxidants are useless. She alone is the key master who permits passage of these antioxidants across the cell membrane. Under the dominion of SREBP, the LDL cholesterol receptor rises to the surface of the cell like a fish rising to feed. If it is lucky, LDL cholesterol will land in its mouth. Along for the ride, precious antioxidants like vitamins A, C, and E are granted access to the cell’s inner world[11].

As this season wanes, berries hang dried and scant on the branches. Insulin recedes as the sugar festival comes to a close. The Earth cools. SREBP breathes a deep sigh as her hard work comes to an end. As she falls into her winter nap, she brings many of the creatures of the Earth with her. Only one creature has successfully escaped the dominion of this goddess. Humans innovated to store carbohydrates externally. This consistent supply of sugar drives insulin to ensure that SREBP never sleeps. Her unrelenting state of slavery drives disorders like obesity[12],[13], fatty liver[14], insulin resistance[15] and atherosclerosis[16], [17]. Perhaps this goddess would argue that these are not diseases at all but are phenotypes brought on by depriving her of a proper rest.

[1] Cutler A.J., Krochko J.E. Formation and breakdown of ABA. Trends Plant. Sci. 1999;4:472–478. doi: 10.1016/S1360-1385(99)01497-1

[2] Teff KL, Elliott, SS, Tschop M, Kieffer TJ, Rader D., Heiman M., Townsend RR., Keim NL, D’Alesso D, Havel Dietary fructose reduces circulating insulin and leptin, attenuates postprandial suppression of ghrelin, and increases triglycerides in women. PJ J Clin Endocrinol Metab. 2004 Jun;89(6):2963-72

[3] Giacomo dugo, Lara La Pera, Donatella Pollicino, marello Saitta. Determination of Selenium Content in Different Types of Seed Oils by Cathodic Stripping Potentiometry (CSP) J. Agric. Food Chem., 2003, 51 (19), pp 5598–5601

[4] Timothy F. Osborne, Peter J. Espenshade Evolutionary Conservation and Adaptation in the Mechanism that Regulates SREBP Action: What a Long Strange tRIP It’s Been. Genes & Dev. 2009. 23: 2578-2591, doi:10.1101/gad.1854309

 

[5] V Laudet Evolution of the Nuclear Receptor Superfamily: Early Diversification from an Ancestral Orphan Receptor. Journal of Molecular Endocrinology Dec. 1, 1997. 19 2-7-226

  • [6] Colleen K. Nye  Glyceroneogenesis Is the Dominant Pathway for Triglyceride Glycerol Synthesis in Vivo in the Rat The Journal of Biological Chemistry, 283, 27565-27574.  October 10, 2008

 

[7] Hitoshi Shimano, SREBPs: physiology and pathophysiology of the SREBP family. The FEBS Journal 2009 276:3 616-621

 

[8] Low Density Lipoprotein Can Cause Death of Islet β-Cells by Its Cellular Uptake and Oxidative Modification Miriam Cnop, Jean Claude Hannaert, Annick Y. Grupping, and Daniel G. Pipeleers Endocrinology 2002 143:9 , 3449-3453 http://dx.doi.org/10.1210/en.2002-220273

 

[9] Zhang C, Chen X, Zhu RM, Zhang Y, Tu T, Wang H., Zhao H, Zhao M, Ji YL, Chen YH, Meng XH, Wei W, Xu DX. “Endoplasmic reticulum stress is involved in hepatic SREBP-1c activation and lipid accumulation in fructose-fed mice.” 2012 Aug 3;212(3):229-40. doi: 10.1016/j.toxlet.2012.06.002. Epub 2012 Jun 12.

“ER stress contributes, at least in part, to hepatic SREBP-1c activation and lipid accumulation in fructose-evoked NAFLD.”

 

[10] Koo HY, Miyashita M, Cho BH, Nakamura MT. Replacing dietary glucose with fructose increases ChREBP activity and SREBP-1 protein in rat liver nucleus. 2009 Dec 11;390(2):285-9. doi: 10.1016/j.bbrc.2009.09.109. Epub 2009 Sep 30.

“Nuclear SREBP-1 was 2.2 times higher in fructose-fed rats than glucose-fed rats.”

 

[11] Maret G Traber, Herbert J Kayden “Vitamin E is Delivered to Cells via the High Affinity Receptor for Low-Density Lipoprotein” The American Journal of Clinical Nutrition 40: October 1984, pp 747-51.

 

[12] Hitoshi Shimano, SREBPs: physiology and pathophysiology of the SREBP family. The FEBS Journal 2009 276:3 616-621

 

[13] Hitoshi Shimano, SREBPs: physiology and pathophysiology of the SREBP family. The FEBS Journal 2009 276:3 616-621

 

[14] Moon YA, Liang G, Xie X, Frank-Kamenetsky M, Fitzgerald K, Koteliansky V, Brown MS, Goldstein JL, Horton JD. The Scap/SREBP pathway is essential for developing diabetic fatty liver and carbohydrate-induced hypertriglyceridemia in animals. Cell Metab. 2012 Feb 8;15(2):240-6

 

[15] Iichiro Shimomura, Robert E. Hammer, James A. Richardson, Shinji Ikemoto, Yuriy Bashmakov, Joseph L. Goldstein,Michael S. Brown

Insulin resistance and diabetes mellitus in transgenic mice expressing nuclear SREBP-1c in adipose tissue: model for congenital generalized lipodystrophy. Genes Dev. 1998 October 15; 12(20): 3182–3194.

 

[16] Karasawa T, Takahashi A, Saito R, Sekiya M, Igarashi M, Iwasaki H, Miyahara S, Koyasu S, Nakagawa Y, Ishii K, Matsuzaka T, Kobayashi K, Yahagi N, Takekoshi K, Sone H, Yatoh S, Suzuki H, Yamada N, Shimano H. Sterol regulatory element-binding protein-1 determines plasma remnant lipoproteins and accelerates atherosclerosis in low-density lipoprotein receptor-deficient mice. Arterioscler Thromb Vasc Biol. 2011 Aug;31(8):1788-95.

 

[17] Kurtak, K. Dietary and Nutritional Manipulation of the Nuclear Transcription Factors, PPAR’s and SREBP’s, as a Tool for Reversing the Primary Diseases of Premature Death and Aging. Rejuvenation Research 17-2. April 2014. P 140-44.

 

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A wise shaman once said, “Don’t confuse compassion with sacrifice. The divine mother is a warrior who is fierce, fearless and full of compassion.” She does not bring forth life into this world with the dainty beauty that has befallen the stereotype of women. She births life as a bloody, ripping warrior whose battle cries reverberate through her body with the echo of a billion lives that came before her. Some made it. Most never survived that journey. Under the escort of Kali, they returned into loving arms of the place from where we all came. And here you stand on this Earth. One of the few whose DNA survived the journey over billions of years. One who survived the War of Nature[1] long before mammals even existed. Who survived famines and floods, droughts and disease, fires, volcanoes, and ice ages. One who defied predation. Much later your genetic material survived tribal wars and world wars, injustices, abuses and epidemics. Your DNA even survived childbirth. Along the journey, your triumphs picked up many friends along the way.

In 1953, Watson and Crick’s discovery of DNA opened our naïve minds to the possibility that life could be as simple as a blueprint. Seemingly endless combinations of codons have been passed from generation to generation from the genesis of life itself. As we sorted through the simplicities of blue or brown eyes, red or blond hair, our genome taught us that an entire existence has come with us that we still don’t completely understand. What we once thought was “junk DNA” was later discovered to be our viral ancestors. One was given the name ERVWE1. Her very presence birthed our own ability to carry out placental development and thus, embryo survival[2].  Through coding for a protein called syncytin[3], she grants sperm and egg another chance to come together for another shuffle of adenine, cytosine, guanine and thymine. Without her, mammalian mothers cease to exist.

Later we discovered completely different type of DNA inside each cell that has nothing to do with the color of our eyes. This DNA resides inside the cell’s mitochondria and enables almost all living beings to convert food into energy. It is a bridge for nutrients between our inner world and Mother Earth. Whether it autogenously developed on its own or came from an ancient bacterium is still a mystery. Unlike the DNA that is passed on from the union of male and female, mitochondrial DNA comes exclusively from the mothers who have passed it through ova from generation to generation.

 

Another universe of genetic material that is passed from the mother is the microbiome. This is “the ecological community of commensal, symbiotic, and pathogenic microorganisms that literally share our body space.”[4],[5]. These various bacteria, fungi, parasites and viruses provide signaling that influences the inner workings of our entire body.   They support immune function, moderate inflammatory responses, generate vitamins that we are not capable of making, produce hormones from some of the foods we eat, help us to absorb minerals, and regulate the production of neurotransmitters. Most importantly, they allow our immune system to remain competitive with the rate of evolution of pathogens.

Comprised of the same creatures found in the Earth itself, this genetic material that we carry inside us has been passed down through thousands of generations. Most animals on the planet, including many (and possibly all) born through eggs[6] receive this life-giving inoculation of Earth as they pass through their mother’s birth canal.

Just a few years ago on February 15th, 2001 we saw our first glimpse of a complete human genome published in the journal Nature. What we thought was a blueprint for solving the mysteries of human disease quickly clouded our concept of the things that us grant us a long and healthy life. Numerous studies appearing in prestigious journals have shown us again and again that genetics plays only a small role in the outcome of our lives[7] [8] [9]. In fact, as little as 10% of our health and longevity is determined by our genetic programming. The rest comes from the daunting myriad of external influences encompassed by entire universes about which we know very little. After all, we’ve only cultured and identified less than 1% of the life within soil, which carries the same microorganisms as our bodies.   The rest is still a mystery. Perhaps understanding them from a scientific basis carries little merit. Wisdom has been passed down in many forms. The original innate wisdom requires no explanation. Its knowledge lies in the very fact that we share this space and time with millions of other creatures whose DNA also survived this epic journey. Because they are here, we are here. Compliments of the fierce compassion of our mothers who carried forth pieces of The Living Goddess.

[1] Darwin, Charles M.A. On the Origin of Species by Means of Natural Selection, or the Preservation of Favoured Races in the Struggle for Life. 24 November 1859. Nature 1st ed.) (London: John Murray) p. 503

[2] Lavialle C, Cornelis G, Dupressoir A, Esnault C, Heidmann O, Vernochet C, Heidmann T. (Aug 2013). “Paleovirology of ‘syncytins’, retroviral env genes exapted for a role in placentation.”. Philos Trans R Soc Lond B Biol Sci. 368 (1626). doi:10.1098/rstb.2012.0507. PMID 23938756

[3] Esnault C, Cornelis G, Heidmann O, Heidmann T (2013) Differential Evolutionary Fate of an Ancestral Primate Endogenous Retrovirus Envelope Gene, the EnvV Syncytin, Captured for a Function in Placentation. March 23, 1013. PLoS Genet 9(3): e1003400. doi:10.1371/journal.pgen.1003400

[4] Lederberg J, McCray AT. ’Ome Sweet ’Omics—a genealogical treasury of words. Scientist. 2001;15:8

[5] The NIH HMP Working Group. 2009. The NIH Human Microbiome Project. Genome Res. 2009 December; 19(12): 2317–2323.

[6] University of Georgia “Healthy Intestinal Bacteria Found Within Chicken Eggs.” Science Daily June 3 2008.

[7] Prof Salim Yusuf DPhil,Steven Hawken MSc,Stephanie Ôunpuu PhD,Tony Dans MD,Alvaro Avezum MD,Fernando Lanas MD,Matthew McQueen FRCP,Andrzej Budaj MD,Prem Pais MD,John Varigos BSc,Liu Lisheng MD,on behalf of the INTERHEART Study Investigators Effect of potentially modifiable risk factors associated with myocardial infarction in 52 countries (the INTERHEART study): case-control study

The Lancet – 11 September 2004 ( Vol. 364, Issue 9438, Pages 937-952 )

DOI: 10.1016/S0140-6736(04)17018-9

[8] Mozaffarian D, Kamineni A, Carnethon M, Djoussé L, Mukamal KJ, Siscovick D. Lifestyle Risk Factors and New-Onset Diabetes Mellitus in Older Adults: The Cardiovascular Health Study. Arch Intern Med. 2009;169(8):798-807. doi:10.1001/archinternmed.2009.21.

[9] Steingraber, Sandra. Living Downstream.   Reading, Mass., Addison–Wesley, 1997 “80% of all cancer is attributable to environmental [external] influences.”(Steingraber, 1998 p 60)

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