Showing posts with label Thyroid. Show all posts
Showing posts with label Thyroid. Show all posts

Monday, March 30, 2015

Gut Guardians Postcast: Episode 16 – (Part 2) Thyroid Help with Robin Treasure

Gut Guardians Postcast: Episode 16 – (Part 2) Thyroid Help with Robin Treasure


Robin Treasure in Part 2 offers her insights on how our guts might play a role in our thyroid health. She advises on the proper testings to diagnose a potential leaky gut causing poor adrenals. Yet another reason to keep your gut sealed up nice and tight.
Be sure to check out Robin Treasures new program ‘Restore!’ to help build and nurture a healthier lifestyle.

Don’t forget to leave any comments or suggestions!
Enjoy!

Show Notes:
Klaire Probiotics


Sunday, August 17, 2014

Sorry. Resistant Starch is Unlikely to Miraculously Cause Weight Loss and Body Fat Loss

Update: Videocast THE SCOOP ON YOUR POOP at 3pm PST Thursday. Please continue to submit questions and I'll answer live and 1-2 that are posted. Thank you!



What's In Your Gut Zoo? Missing Leanness and Longevity?

If you are plateauing on fat loss, consider the gut microbes that can hijack and hamper your health success. The 5 mass extinctions of the gut microbiota lead to the loss of 'the limbs of the microbiota' that are attributed to leanness and longevity.

Consider that we co-evolved with them for millions if not billions of years and it is a relationship that requires nurturing, replenishment, and proper attention. Consider that for optimal body fat recomposition, the bugs residing/missing in the gut may be more important than the fuel. You may be feeding empty zoo cages in the modern age or worse, caged vipers, rogues and renegades.


Resistant Starch is Highly Unlikely to Miraculously Lead to Fat Loss

Recently Dr. Nett at Kresser's office did a post about how raw starch RS2 may improve weight loss. How resistant starch (RS) can help is very very very indirect. Let's talk about the entire community of the gut and c-o-n-t-e-x-t.

I have not seen raw starch RS2 miraculously induce fat loss in obese human animals. I can list the people who are still 'challenged' (like I was for a while!).  Unfortunately there are few anecdotes, human RCTs, human cases or internet stories that back up instant weight loss with raw starch RS2 -- yes -- because I've looked.  RS is just a fiber. Digestible complex carbs are fiber too -- 10% escape into the colon and feed the microbiota quite well. If the diet is 150-200 grams carbs, then 15 to 20 grams will be pure fuel for the colon flora. Nice, eh? That's half of our 'fiber quotient'.

If you want to lose weight and break body fat plateaus, the fuel and fibers for the flora that have evidence of successful human trials and RCT outcomes are:
--arabinoxylan (psyllium, whole GF grains)
--pulses (legumes = rich in phytochemicals, RS3, fibre, protein, minerals and vitamins)
--oat bran
--beta glucan (carrots, celery, radish, oats, mushrooms)
--glucomannan, konjac, etc.


RS has none ...and coprophagic rodent studies don't count. So much promise, no teeth.

All fiber is not created equal.



Sorry. Raw Starch RS2 Alone So Far Has No Weight Loss Results in Human Studies

These researchers Johnston et al found "Resistant starch consumption did not significantly affect body weight, fat storage in muscle, liver or visceral depots. There was also no change with resistant starch feeding on vascular function or markers of inflammation. However, in subjects randomized to consume the resistant starch, insulin sensitivity improved compared with the placebo group (P = 0.023)...Unlike in animal models, diabetes prevention does not appear to be directly related to changes in body adiposity, blood lipids or inflammatory markers. Further research to elucidate the mechanisms behind this change in insulin sensitivity in human subjects is required."

Low (15g) and high dose (30g) RS2 for 4 weeks didn't induce fat loss either but improved insulin resistance in obese men, not women (Maki et al, 2012).

Neither did 25 grams refined RS3 supplementation (Novelose330), but high-protein/40% carbs resulted in all body fat parameters pivoting: improved insulin sensitivity, body fat loss and weight loss in human subjects with metabolic syndrome (Lobley et al, 2013).

Neither did 40 grams RS2 supplementation for 12 weeks in T2 diabetes (Bodinham et al, 2014). Strikingly, this study also showed that HAM-RS raised triglycerides in a statistically significant manner and failed to lower body fat, Hgba1c, blood glucoses or improve central insulin resistance at the liver.

(However, a whole food supplement which contains a broad spectrum of microbial superfoods, native banana starch flour (NBS) 24 g/day induced 1.2 kg weight loss, improved waist-hip ratios and insulin sensitization in T2 diabetic, obese females after 4 weeks, contained only 8 grams RS2 (Ble-Castillo, 2010). Version B of BIONIC FIBER in the 7 steps. Green banana and plantains have been shown to heal ulcers and infectious colitis.)



Root Causes of Excessive Fat Gain and Obesity

What does work is getting to the root causes of obesity, fat gain and dysregulated metabolism. Humans are complex. Obesity and evolution are intertwined. For all life on earth including plants and insects, we are superorganisms living in symbiosis with an entire community of microbes. The microbial community can actually hijack and hamper health when it is diseased. OTOH the microbial community can be epically collaborative in optimizing longevity and health in our co-evolved microbe-host interaction that has been ongoing for literally hundreds of millions of years, if not billions.

Many examples of a collaborative community exist where mutual support and mutual exchange of energy and spirit co-exist. Local, sustainable, organic farms that bring our livestock, eggs and produce are my favorite examples. The paleo/primal hood and the ancestral AHS14 are others.

Fighting Obesity With Bacteria
Hat tip: M


Body Fat Reduction: Mice Cohousing and Ancestral Core Bacterial 'Invasion'

I talked about the cohousing experiment by Ridaura et al at AHS. They took gut microbiota from human twins that were discordant for obesity (one twin lean, one twin obese) and put them into GF (germ free) rodents. Later they cohoused lean with obese mice and observed the changes after a fat inducing diet (high saturated fat) v. high fiber, low fat diet. The results were not surprising and showed the compelling power of poop. Why did cohousing work?

(Coprophagy = PROBIOTICS)

On the fat inducing diet, lean mice didn't get as obese and the obese mice become super obese.

On the higher plant polysaccharide diet (LoSF-HiFV), both the obese and lean controls naturally had improvements in body fat recomposition. The lean controls loss fat mass (and some lean mass). The obese controls loss fat mass and gained lean mass.

See below. The cohoused animals had notable changes which make this study an epic study for the gut: the lean cohoused mice got jacked by eating the poop of the obese mice, eg they gained fat mass on the high fiber diet. The obese mice however upon cohousing, high plant fuel diet, and attaining the 'lean core microbiota' (mini fecal transplant) via coprophagy/cohousing GAINED LEAN MASS AND LOST SIGNIFICANT BODY FAT MASS.

I think the true beauty of the Ridaura study is that the shift in microbiota + diet reflected in metabolic changes, insulin sensitivity and body fat recompositioning. The gut shifts were tracked and the invasion of the ancestral core microbes from the lean mice into the obese mice was directly related to the body fat changes.


Ridaura et al 2013
LoSF-HiFV, low fat high fiber diet

Healthy Invasion of the Core LEAN Human Gut Microbiota

Fig 3A and 4C shows the shift in the gut that correspond to the lean phenotype. The roadmap to healthy body fat recomposition is shown here. An 'invasion' of the lean 'poop' (mini fecal transplant) into the obese mice are dissected into just a handful of species, of which two are part of the ancestral core that I talk about at AHS. All the species below are great when they are coming from a 'healthy community' eg happy, healthy, horny/hormonally-young mouse.

Enriched in mice colonized with or  invaded by members of a Ln microbiota
Bacteroides uniformis*
Bacteroides vulgatus* -- one of the 7 ancestral core
Eubacterium desmolans* -- E. rectale is one of the 7 ancestral core
Parabacteroides merdae*
Alistipes putredinis* -- one of the 7 ancestral core
Ruminococcus callidus
Ruminococcus bromii -- one of the 7 ancestral core
Clostridium symbiosum
Roseburia unclassified -- one of the 7 ancestral core
Clostridium ramosum
Akkermansia muciniphila ~~ high in hawwt, high lean mass rugby players w/low inflammation
Ruminococcus obeum
Ruminococcus sp. 14531
Eubacterium ventriosum
Betaproteobacteria unclassified
Burkholderiales unclassified
etc


Here's the 7 core ancestral microbiota based on Julien Tap's work:

Actinobacteria 
Bifidobacteria longum

Clostridia cluster IV
F. prausnitzii
Ruminococcous bromii 

Clostridia cluster XIVa
Roseburia intestinalis
Eubacteria rectale

Bacteroidetes
Bacteroides vulgatus
Alistipes putredinis




To Lose Epic Body Fat: My Top 10 E≠MC2

1. Fix your lovely gut (1/3-1/2 will do well with my 7 steps which both Dave Asprey and Mark Sisson have tried)

2. Introduce lean-gut-like probiotics (Prescript Assist, Body Ecology, ThreeLac, smoothies with organic dirty beets, letting your lean dog lick you, working at organic farms, etc)

3. Raise your metabolism
--exercise, yes move your cute *ss instead of standing on body vibrators, consider ten thousand steps daily

4. Raise your metabolism
--fix your adrenals and anabolic hormones (both men and women need progesterone and testosterone and titrated estrogen; get the anabolic up, get the estrogens down. detox xenoestrogens that make your moobies grow and cause cancer, inflammation and difficult to battle body fat)

5. Raise your metabolism
--lowering mental/emo inflammation by embracing being happy, optimistic, and grateful; flooding yourself with oxytocin (hug, hold, kiss your family and friends)

6. Raise your metabolism
--fix hypothyroidism (iodine, selenium, exercise, remove mercury, don't over-exercise, sleep well, avoid ketosis if increasing peripheral insulin resistance)

7. Feed your gut well
--plant fibers, the whole spectrum of ancestral fibers (roots, onions, leeks, tubers, beets, carrots, legumes, gluten-free soaked grains)

8. Plant polyphenols lower inflammation as well as tighten up gut epithelium and tight junctions (bilberry, citrus, pectin from legumes and apples, etc)

9. Lower non-ancestral stress

10. Weed your gut
--probiotics
--fiber, complex carbohydrates (low glycemic index), resistant starch
--in obesity, several overgrowths have been detected with consistency and reliability. Get ride of these. The species are listed in Ridaura's article and my AHS14 slides. The lean mice (from human discordant twins) do not have these strains and when they were invaded, they gained body fat even on the high fiber low fat diet. In human gut sequencing studies, overgrowths of yeasts, protozoa, parasites and pathogenic bacteria are found. Fix these by seeing an integrative and functional medicine practitioner for stool/urine testing and appropriate care

Tuesday, April 16, 2013

Babies and Mapping the Pollution in People: EWG's HUMAN TOXOME PROJECT

I think this is cool (...naught really).

This is a (user-friendly) compilation of the data collected in individual and large studies by the Environmental Working Group's Human Toxome Project. You can click on the right side on the study or an individual to review the toxic metals, pesticides, solvents, PCBs, POPs, and other chemicals found and at what level (low, mod, high).



The data below is from the EWG/Commonweal Study #1.



In each of these 9 adult participants over 150 chemicals, pesticides, solvents and heavy toxic metals were found. Fifty chemicals and metals that have been shown to cause dysfunction of the immune system were detected.  I talked about these factors above at AHS2011 'Rainforest of Your Gut' because not only do they disrupt our immunity but also intestinal barriers and permeability.  Researchers estimate that the intestinal system contains 70-80% of the immune cells.  Once chronic intestinal permeability occurs, all hell breaks loose.  Signs can be acute or terribly subtle....Bloating, dyspepsia, heartburn, hormonal disruptions (men become fem/moobies and grrrrls masculinize), inflammation, insulin resistance, suboptimal adrenals/thyroid, low HDL/high LDL, heart disease, endothelial hardening, penises softening, mental vulnerabilities, autoimmunity, autism spectrum, skin disorders, sinus disorders, candida overgrowth, allergies, oxidative DNA damage, and 50 Shades of F-Cked (cancer).

How do all these multiple industrial neolethal toxic factors influence our health?  From a systems biology perspective, do multiple factors amplify the depth of damage as each organ system one-by-one fails to accomplish what it is designed to do?

People eat whole foods, filtered water, organic, sustainable, ancestral, paleo, et cetera, but is it enough?  What if an individual has a low exposure but genetic variants for particular detox/antioxidant pathways which keeps an industrial toxin or metal hanging around? ApoE4, COMT, MTHFR, MT, and GST are just a few. Granted most of us have decent flux and adaptive mechanisms to survive most assaults but what are the thresholds for coping for multiple exogenous assaults combined with unique endogenous frailities?

On the other hand, what if a person just gets an accumulated butt-load of low exposure from frequent or daily soaked, arsenic- or lead-laced brown rice or heart-healthy omega-3 mercury/flame retardant- and selenium rich wild seafood?  Sorry -- I don't buy that urban mythology.

When I used to go for miles and miles jogging in the neighborhood, on weekdays I watched unprotected city workers spraying pesticides and herbicides on grass edges and around the municipal parks. Where does all the herbicide water run-off go? Where do contaminated water sources originating from Big Agro GMO Monsanto crop fields end up?  How is it tracked? Why not?

67% of the 9 individuals had 'high levels' of mercury detected and 22% 'low levels'.  Mercury used to be in our mouths; my kids and I are amalgam-free for one year now. We rarely eat wild fish with our histories and above is why.

Fukushima radiation is another now (here and here).

Before a first breath of air, 10 babies via cord blood lab analysis (EWG study #4) were found to have 287 heavy metals, pesticides and chemicals. All 10 had mercury (60% moderate levels, 40% low). 100% had dioxin. 100% had PCBs. 100% had organochlorine pesticides.





Recently pesticides from Bt GMO crops were found in 80% of fetuses and 93% of adults (healthy pregnant) randomly tested in one Canadian study (Aris and Leblanc, Reproductive Toxicology, 2011). This herbicide is used as a topical spray as well genetically spliced into the DNA of GMO crops with promoters for high-copy amplification and expression of of a bacterial toxin bacillus thuringiensis (Bt). Bt toxin is also known as Cry1Ab protein.  It is a gut specific delta-endotoxin which exerts toxicity through increasing larvae/insect intestinal permeability causing the death of crop pests like leaf- and needle-feeding caterpillars (lepidopteran insects --butterflies, moths), beetles (coleoptera--weevils, ladybugs, beetles), and the larvae (e.g. babies) of leaf-beetles. It has been designed to be toxic to mosquitoes (dipteran)now.  Fun, no?

Has lateral transfer of Bt DNA to our gut bacteria and microbial communities already occurred (or at least the unborn and adult Canadians in Aris and Leblanc's study)?  Are we transformed? Mutant gut-hybrids of GMO experiments gone awry?

Like advising pregnant moms to avoid fish and seafood to minimize exposure to bioaccumulation of mercury and other pollutants, the American Academy of Environment Medicine (AAEM) issued a GM Foods Position Paper on May 8, 2009 for everyone to avoid all GMO foods in their diets.  Why such adamant recommendations for exclusive GM-free diet prescriptions?



For physicians and healthcare practitioners, they encourage looking at the role of GM foods in health disorders and diseases in integrated medical evaluations.  Why are we fat?  Why does USA obesity trends track and follow herbicide use?  Why are hypothalamus and brain reward centers so SO BROKEN?  How is the global use of herbicides and Bt gut-perforating pesticides related to our health woes and epidemic cancer and diabesity/heart disease/strokes?



In 1998 two scientists fed mice for two weeks potatoes (a) soaked for 30min in a dilute suspension of harvested Bt toxin (from bacterial spores grown in the lab; 1 g/L concentration), (b) transgenic Bt potatoes, and (c) control potatoes. Mild structural changes in the microvilli of the ileum of the transgenic GMO Bt potatoes were seen in.However in the Bt delta-endotoxin soaked potato-fed mice, the ileum changes were quite substantially greater in scale -- '...basal lamina along the base of the enterocytes was damaged at several foci. Several disrupted microvilli appeared in association with variable-shaped cytoplasmic fragments.' The authors further report 'in the group of mice fed on the delta -endotoxin-treated potatoes, the Paneth cells of the crypts of Lieberku¨hn were highly activated and contained a large number of secretory granules. These cells are believed to have an important role in the activation of phagocytes and controlling the bacterial flora of the gut (Ariza et al., 1996; Fawcett, 1997). They contain elevated levels of lysozyme in their large eosinophilic secretory granules, an enzyme capable of digesting bacterial cells walls, and antibacterial peptides called cryptdins (Junqueira et al., 1998). Ouellette (1997) revealed that Paneth cell secretory products seem to contribute both to innate immunity of the crypt lumen and to defining the apical environment of neighboring cells....The antimicrobial polypeptides of the Paneth cell secretory products kill a wide range of organisms, including bacteria, fungi, viruses and tumor cells (Aley et al., 1995).'  Lysozymes are 'cutters' -- they cleave and cut things, for instance, tumour/cancer cells and cell walls of pathogens that take a ride in our food.

Damage to the ileum and small intestines can lead to changes in microbial population and the disorder known as SIBO (small intestinal bowel overgrowth).  An expanding body of knowledge links SIBO with nearly every chronic systemic and skin disease seen in outpatient medicine (John Hopkins Turnbull, Mullin et al)

Bt toxin appears to induce self-digestion -- (increased Paneth cell and lysozymal activity) and damage from the inside out.  Lovely! And it is present in unborn children and adults.




References

Nutrient tasting and signaling mechanisms in the gut. II. The intestine as a sensory organ: neural, endocrine, and immune responses.
Furness JB, Kunze WA, Clerc N.
Am J Physiol. 1999 Nov;277(5 Pt 1):G922-8.

Adult Women’s Blood Mercury Concentrations Vary Regionally in the United States: Association with Patterns of Fish Consumption (NHANES 1999–2004)
Kathryn R. Mahaffey, Robert P. Clickner, Rebecca A. Jeffries
Environ Health Perspect. 2009 January; 117(1): 47–53.

Blood mercury reporting in NHANES: identifying Asian, Pacific Islander, Native American, and multiracial groups.
Hightower JM, O'Hare A, Hernandez GT.
Environ Health Perspect. 2006 Feb;114(2):173-5.

Pesticides in Shanghai and Globally

Pesticides May Cause USA Insulin Resistance and Obesity Trends

Maternal and fetal exposure to pesticides associated to genetically modified foods in Eastern Townships of Quebec, Canada. (FREE PDF)
Aris A, Leblanc S.
Reprod Toxicol. 2011 May;31(4):528-33.

Fine structural changes in the ileum of mice fed on delta-endotoxin-treated potatoes and transgenic potatoes [GMO Bt toxin] Free PDF
Fares NH, El-Sayed AK.
Nat Toxins. 1998;6(6):219-33.

Principles of Integrative Gastroenterology, Systemic Signs of Underlying Digestive Dysfunction and Disease, Turnbull, Mullin, et al.

Assessing Cumulative Health Risks from Exposure to Environmental Mixtures—Three Fundamental Questions
Ken Sexton, Dale Hattis
Environ Health Perspect. 2007 May; 115(5): 825–832.

Combined toxic exposures and human health: biomarkers of exposure and effect.
Silins I, Högberg J.
Int J Environ Res Public Health. 2011 Mar;8(3):629-47.

Thursday, November 8, 2012

Mitochondria: Fuel, Fluxxx and Heat (NSFW)

Buddha Bar (Sex Lounge)
Credit: Youtube.com



Fuel and Fluxxx...

Why do we store fat? Why do we eat?  A scientist who wrote about reproduction, fuel, photoperiods and fecundity wrote the below abstract...[1]

"While there is a relatively direct connection between
circulating levels of metabolic fuels and the GnRH [gonadotropin releasing hormone] pulse generator [in SCN behind the retina], this might not be the only energy-related pathway influencing the secretion of this neuropeptide. The overall control of energy balance is an immensely complex process and a number of pathways involved in it might secondarily influence the activity of GnRH neurons. Peripheral signals influencing energy balance and thus possibly GnRH secretion could come from the liver, pancreas, stomach, duodenum or adipose tissue, and these signals could be sent to the brain via the vagus nerves or by hormones such as leptin, insulin, insulin-like growth factor 1 or ghrelin. These hormones could act directly on the neural circuits controlling the GnRH neurons or they could act by modulating the availability of metabolic fuel. Likewise, the neuropeptides regulating GnRH secretion in the forebrain could also include galanin, orexin, the urocortins and endogenous opioids. Recent interest has focused on kisspeptin, the product of the KISS1 gene. The presence of kisspeptin is necessary for normal reproductive development and it can override the reproductively detrimental effect of mild food restriction."

Obviously how we expend fuel is highly complex and humans are ruled by a big, big, big, hungry, hot brains... Grow or growl? Feast or fast? F-ck or forage? Repair or repast?





HEAT: Cellular Bioenergetics Creates Wildly Explosive, Exothermic Reaction Generating Water



CALORIES IN  ≠  CALORIES OUT

...we are not neat bomb-calorimeters, but open, conserved, networked metabolic and energy systems...

Photos credit: [2].













The Evolution of Body Heat?

When oxidized, the great majority of our food and stored energy goes to the production of HEAT.      What governs this? It is multifactorial but adrenaline, thyroid, cortisol and mitochondria quality are just a few [2]. Active tissues contain more mitochondria. Heat makes us mammals and birds. We have hot bodies, precisely 37C for the great majority.


In the 'Hot Brain:  Survival, Temperature, and the Human Body' the authors theorized that temperature gave us advantages over eukaryotic infections (yeast, fungal origins -- we are eukaryotic) which plagued bird/reptile species which were not armed with high 37C temperatures or fever-inducing capabilities [3].  It is a very interesting theory. Control of thermoregulation (heat loss v. heat gain) is believed to have evolved in the brain of therapsids. Our sinuses are larger. Mammalian brains have a Circle of Willis where 4 arteries (internal carotids and vertebral arteries) provide a complete internal brain circulation with collaterals, such that despite blockage of one or more of the 4 major arteries circulation in the brain and to the body remains intact.  Unfortunately only 25-33% of us have a 'perfect' classic circle of Willis; others have degrees of narrowing or asymetry in certain areas or another. Photos courtesy: Hot Brain, pp. 44, 142.

Recently a microbiologist, Casadevall, from Albert Einstein had the same theory that the rise of mammals can be attributed to 'endothermy and homeothermy [which] are thought to contribute to mammalian resistance to mycosis by creating a thermal exclusionary zone that inhibits most fungal species. The remarkable resistance of mammals to mycotic diseases is probably a combination of a vertebrate immune system, with both innate and adaptive arms, and elevated body temperatures... The currently favored hypothesis for the demise of dinosaurs and end of the age of reptiles is a bolide impact approximately 65 million year ago with the possibility that other events, such as increased volcanism, contributed to disrupting the cretaceous ecosystem. That ecological calamity was accompanied by massive deforestation, an event followed by a fungal bloom, as the earth became a massive compost. Although one cannot know which spores were present at the time, the likelihood that pathogenic fungi existed at the K-T boundary is enhanced by the finding that the potential for pathogenicity probably arose independently several times in evolution...'[3]

'Although we do not know the timeline for the recovery of the planet climate, it is estimated that photosynthesis was shut down for 6 months and climate cooling persisted for at least 9 years, and the occurrence of a fungal bloom sufficient to have left fossil evidence implies that surviving animals were exposed to massive numbers of fungal spores. The darkened skies and cooler temperatures that accompanied the K-T cataclysm would have shielded the sun and reduced the ability of ectothermic creatures such as reptiles to induce fevers by insolation, a necessary activity for protection against fungal diseases. Hence, it is reasonable to posit that ectothermic creatures unable to induce behavioral fevers and in weakened states from environmental stress would have been at a severe disadvantage relative to small mammals with their innate thermal exclusionary zones for fungal growth. Further complicating the situation for reptiles is that eggs can be vulnerable to fungal attack, whereas mammalian progeny would be protected in placentae.'[3]

I think it has merit. We generate a lot of HEAT and it comprises a cr*pload of our total energy losses (as many in NY know without electricity due to Storm Sandy and no heat to fight night time drops to freezing temperatures). As Casadevall reported  'the mammalian lifestyle is energetically costly.'






Mitochondria: Water (H2O) = 286 kJ of P-O-W-E-R

Many obesity researchers appear to forget these multiple evolutionary and hormetic factors in their Big Pharma funded, tenure-track equations. One did not (though partly Joslin funded which is Big Pharma).


In a Nature article, Tseng et al discuss mechanisms to find a drug target to increase cellular bioenergetics and energy expenditure as an anti-obesity strategy [2]. (But... Drug targets are always silly, no?) They discuss PPAR-delta, AMPK and several other pathways with potential promise.  A succinct explanation of how mitochondria produce energy on demand by harnessing the energy from the formation of water in the cellular bioenergetics of mitochondrial metabolism of fuel is provided. They define bioenergetics as the 'Studies the flow of chemical bond energy within organisms. In a living cell, the principal reactions of fuel metabolism take place in the mitochondria, where food energy is released,oxygen is consumed, and water and carbon dioxide are produced.'

All life on earth utilizes the energy formed from water formation to power pathways and metabolism. Remember the Calvin Cycle/Photosynthesis where carbs (glucose) are formed from air (CO2), and energy of the sun? In the mitochondria, the opposite reaction occurs. Energy from the exothermic reaction of water forming from air (O2) and the enzymatic burning of fuel (oxidizable food, glucogen, glucose, fat) result in HEAT and ATP. When one mole of H2O is created from one H2 (hydrogen) and half O2 (oxygen), 286 kJ of power are released (in other words, 68 kcal, which is about one small potato).... FROM FORMATION OF ONLY ONE MOLE OF WATER.

CO2 1/2 O2  =   one mole H2O (~18 grams water = 3.5 teaspoons)  =  286 kJ






Fuel Efficiency of Our Mitochondrial Cellular Respiration

With cellular respiration, instead of an enormous, exothermic explosion (like a hydrogen bomb), the electrons and protons are added step-wise on a gradient known as the electron transport chain (ECT) in plants and animals.  A biological mitochondrial 'battery' is created with the 'anode' on the inner mitochondrial membrane side and the 'cathode' on the other.  Heat is energy released when oxygen is the final proton acceptor and coupled to the enzyme (F1F0-ATPase) that forms ATP, the universal currency of cellular energy in the body. When the protons fall across the proton channel, ATP is formed.  We use ATP as fuel every minute every day for all cellular work, then recycled back to ADP.  In one day, it is estimated that our mitochondria may produce our own weight in ATP [5].

Efficiency of the theoretical transfer of energy from oxidizable fuel to ATP and heat is pretty darn good: 39% ATP and 61% heat [5]. Mitochondria are energy rockstars. Obviously many biolgical factors determine true efficiency: iron status (cytochromes are composed of heme), ubiquinol, oxidative and inflammatory state, thyroid, HPA axis function, hormones, etc.

Plants (chloroplasts) get 3-6% efficiency from transfer of solar energy to the energy bonds of plant starches and fatty acids. Particular C4 plants can get 7-8% (sugarcane) and one super cyanobacteria strain Chlorobaculum tepidum achieves 10%. Various modern fuel efficiencies are approximately -- for coal (~20-30s%) and solar (20%). Photo credit: [5].



References

1. Climate change and seasonal reproduction in mammals. Bronson FH.Philos Trans R Soc Lond B Biol Sci. 2009 Nov 27;364(1534):3331-40.

2. Cellular bioenergetics as a target for obesity therapy.Tseng YH, Cypess AM, Kahn CR. Nat Rev Drug Discov. 2010 Jun;9(6):465-82. [Free PDF here]

3. The Hot Brain: Survival, Temperature, and the Human BodyCarl V Gisolfi, Francisco Mora Teruel. MIT Press (Bradford Book), 2000. [Free SCRIBD text here]

4. Fungi and the rise of mammals.Casadevall A. PLoS Pathog. 2012 Aug;8(8):e1002808.  [PDF]

5. http://highered.mcgraw-hill.com/sites/dl/free/0073525502/930160/mad25502_ch08.pdf

Monday, November 5, 2012

Phat Fat Mitochondrial Energetics: Mobilization v. Accumulation


Adipose is Alive

In ancestral times, adipose stores may have determined longevity and survival past harsh cold winters. My ancestors moved from northern China 8-10+ generations ago to the mountainous areas of Taiwan (according to my dad several hundred years ago). I suppose those who didn't live past the impoverished seasons where food resources were scarce would not have made it, nor would their genes. I can thank them for my persistent fat stores *haa*. Adipose tissue is an endocrine gland which is know to secrete hormones such as leptin and adiponectin to control hunger, body energy balance and energy expenditure. These hormones are involved directly with mitochondrial biogenesis as well, in other words the production and destruction of the mini powerhouses found in all cells (except perhaps glycolytic-dependent cancer cells, which I think are all of them).

Whole body energy balance are determined by many factors, including most importantly:
1) demand
2) diet
3) d*ng hormones (or lack of)



All Organs Sync For Survival

Our brain coordinates many of the hormones that either mobilize or store adipose, e.g. fat. The brain includes the hypothalamus, pituitary, pineal, forebrain, hindbrain, midbrain and our senses for perception (ears, eyes, nose, taste, temperature, barometric pressure, etc). For example, insulin is triggered cephalically (via the brain): by tasting sweetness whether artificial or real, by smelling food, seeing food or even imagining food. Hearing? Hearing the neighborhood ice cream truck as a kid?




Humans Killed for Fat

Fat may have been the biggest boon for man during evolution (see prior animal pharm: humans as marine-based carnivores). Fat contained omega-3s concentrated up the food chain from green chlorophyll sources (grass, algae, etc) and into the muscle fat, organ meats, brains and fat stores of animals and seafood. The encephalization of ancient man is believed to be highly associated with the intake of dietary omega-3s. Perhaps the current de-encephalization over the last 100 yrs is related to the relative deficiency of dietary omega-3s? Or growing overabundance of omega-6s? THANK YOU VERY MUCH corn-fed cows and Keys.




Fat Yields the Most Energy in Human/Mammalian Energy Systems

Hormones for MOBILIZING fat stores far out number the hormones that ACCUMULATE fat. See diagram, modified from Gary Taubes GCBC from a 1965 table of hormonal regulation. Forgive me I use the term 'hormone' loosely because food is hormonal. Fatty acids bind PPAR receptors. We have ~ 3-4 routes to produce energy (some cells utilize glutamine, but I don't know which... neurons only?). Burning fatty acids yields the highest net energy unit (ATP). Why I've wondered? So many hormones promote the escape of fatty acids from temporary storage -- intramuscular, liver, visceral fat, brown fat and subcutaneous fat. Why do we readily release fatty acid energy? Sex, power, survival/suicide? Heat for 37C?

Taubes quoted Hans Krebs who received the Nobel in Medicine in 1953 'All three major constituents of food supply carbon atoms.. for combustion." GNG= gluconeogenesis (glucose/glycogen from any source -- protein, fat, carbs); ATP lesson (click HERE and UCD Lecture and med biochem):



Low Yield but Mandatory Without Oxygen
--anaerobic glycolytic (glucose/GNG) [Yield: 2 ATP]


High Yield in the Presence of Oxygen
--aerobic glycolytic (glucose/GNG) [Yield: 38 ATP] 
--aerobic beta-oxidation of fatty acids like palmitate [Yield: 129 ATP]
--aerobic beta-oxidation of fatty acids like stearate [Yield: 146 ATP]
--aerobic beta-oxidation of fatty acids like ketones [Yield: 51 ATP]
--aerobic oxidation of alcohol [Yield: 16 ATP]


Carbon lengths:
Glucose: 6-carbon carb
Palmitate: 16-carbon saturated fatty acid
Stearate: 18-carbon saturated fatty acid
Ketones (b-oh-butyrate, Ac-Acetate): 4 carbon fatty acid
Alcohol: 2-carbon 'the fourth food group' *haa* tequila is paleo, no?

Prior animal pharm: Palmitate Utilized Between Meals




Mitochondrial Medicine

Where does all this high energy production occur? Of course. Your mitochondria (the lower-net-energy anaerobic pathway is independent of mitochondria, occurs in the cytoplasma).

So. Don't scr*w up your mitochondria. That's like jacking your ride. Blowing out your carburetor.

...FLUNKING your human SMOG TEST.

Mitochondrial medicine is a new field but old premises still apply. The paleo evolutionary paradigm for which your mitochondria and DNA were perfected and honed over 2.5M years of natural and sexual selection are what we believe optimize health and maximize vitality.

Sunday, May 31, 2009

Become B-I-O-N-I-C


Hormesis...and cold showers...

I should... *ahaaa* more often (besides tri-training)

As I wish I could shut my playboy mouth...(Lady Gaga)

Mark Twight, founder of Gym Jones and former-Xfitter, was the coach hired to whip the '300' Movie actors and stuntmen into astounding warrior-shape. He employs several techniques to induce hormesis.

One technique: C O L D S H O W E R S (WSJ article, Training That's Beyond Boot Camp by Mr. M. Ybarra)
Other techniques: Mr. Cosgrove, '300' Workout


A researcher in Denmark, Dr. S. Rattan, has written about the benefits in extending lifespan via hormesis (Ageing Res Rev. 2008 Jan;7(1):63-78). "Hormesis in aging is represented by mild stress-induced stimulation of protective mechanisms in cells and organisms resulting in biologically beneficial effects. Single or multiple exposure to low doses of otherwise harmful agents, such as irradiation, food limitation, heat stress, hypergravity, reactive oxygen species and other free radicals have a variety of anti-aging and longevity-extending hormetic effects. (me thinks the torture umm... the WODs at X-fit fit this definition) Detailed molecular mechanisms that bring about the hormetic effects are being increasingly understood, and comprise a cascade of stress response and other pathways of maintenance and repair. Although the extent of immediate hormetic effects after exposure to a particular stress may only be moderate, the chain of events following initial hormesis leads to biologically amplified effects that are much larger, synergistic and pleiotropic. A consequence of hormetic amplification is an increase in the homeodynamic space of a living system in terms of increased defence capacity and reduced load of damaged macromolecules. Hormetic strengthening of the homeodynamic space provides wider margins for metabolic fluctuation, stress tolerance, adaptation and survival. Hormesis thus counter-balances the progressive shrinkage of the homeodynamic space, which is the ultimate cause of aging, diseases and death. Healthy aging may be achieved by hormesis through mild and periodic, but not severe or chronic, physical and mental challenges..."


Brief cold stress appears to improve our immune systems by stimulating the hypothalamic-pituitary-adrenal and hypothalamic-pituitary-thyroid axes as described HERE research is reviewed including an experiment where T. gondii-infected-rats had improved survival with cold-hydrotherapy x8days.

Exposure to periodic, repeated, short term (like 2-7mins) cold stress induces hormesis which can help to rebuild and regenerate our bodies and minds... making us... stronger, better, more powerful...

B I O N I C .


And...BTW make sure you don't consume too much sucrose (carbohydrates) and make sure you have healthy adrenal function (good quality/quantity sleep, reduced mental stress, adrenal support if needed, etc), otherwise the beneficial stress-responses will be shut down:
Sucrose intake and corticosterone interact with cold to modulate ingestive behaviour, energy balance, autonomic outflow and neuroendocrine responses during chronic stress.
Bell ME, et al. J Neuroendocrinol. 2002 Apr;14(4):330-42.



Dr. W. Bushell from MIT wrote a review called "From molecular biology to anti-aging cognitive-behavioral practices: the pioneering research of Walter Pierpaoli on the pineal and bone marrow foreshadows the contemporary revolution in stem cell and regenerative biology" in 2005 (Ann N Y Acad Sci. 2005 Dec;1057:28-49). Stem cells are the backbone of rebuilding organs and other body parts. He suggests that a revolution is going on in medicine and science... ya think...???

Evidence is accruing that a cognitive-behavioral regimen integrating cognitive techniques (meditation-based anti-stress, anti-inflammatory techniques, others), dietary modification ("dietary restriction" or modified dietary restriction), and certain forms of aerobic exercise, may prolong the healthy life span in humans. Recent research has identified some of the likely molecular mediators of these potentially broad-ranging, health-enhancing and anti-aging effects; these include DHEA, interleukins -10 and -4 (IL-10, 1L-4), and especially melatonin. Relatedly, what some are calling a revolution in biology and medicine has been emerging from research on stem cells and regeneration processes more generally.

Dogma regarding limitations on the regenerative capacities of adult vertebrates is being cautiously yet enthusiastically revised in the wake of rapidly accumulating discoveries of more types of adult stem cells in mammals, including humans. For example, a recent review by D. Krause of Yale concluded that "in the [adult] bone marrow, in addition to hematopoietic stem cells and supportive stromal cells, there are cells with the potential to differentiate into mature cells of the heart, liver, kidney, lungs, GI tract, skin, bone, muscle, cartilage, fat, endothelium and brain." In addition, very recent studies have shown that DHEA, ILs-10 and -4, and melatonin all possess potential regenerative, including stem cell-activating, properties.

More than a quarter of a century ago, Walter Pierpaoli initiated a series of extraordinary studies that demonstrated in experimental animals the potential for dramatic regeneration associated with changes in the pineal gland and bone marrow. This appeared to be not only retardation of aging, but also its REVERSAL.

Furthermore, as Pierpaoli was attempting to understand both anti-aging regeneration and oncogenesis, he was focusing on both pro- and anti-mitotic mechanisms: recent research now suggests that there is a nonpathologic, "healthy" form of regeneration that is actually antagonistic to oncogenesis, and that melatonin may be important in this form of regeneration.


This paper explores Pierpaoli's pioneering studies in light of recent developments in stem cell and regenerative biology, particularly as related to the regenerative potential associated with certain cognitive-behavioral practices, and includes evidence on this subject presented for the first time.

Prior relevant animal pharm posts:
Melatonin: Evoke Tranquility
Thyroid: Hormonal Imbalances
Bone Marrow: Immoprotective and Improves Endothelial Function

Monday, February 16, 2009

Animal Pharm Science: Vitamin A Deficiency Increases Marbling


Do you want marbling in your meat? I mean, fat-infiltration of your meat-muscles...biceps, triceps, quads and gluts.

M-A-X-I-M-A-L gluteus maximus is what I'm going for! Maximization with functional exercises like squatting and digging volleyball-style which is oh-so-nice...

Not... marbled...meat!!

Looking at journals of animal farm science, studies for increasing USDA Grades of beef and Marbling Scores (MS) have yielded some interesting perspectives regarding vitamin A and its role in controlling obesity. Do Americans get enough vitamin A? The beef industry has figured out that better grades and thus higher market value can be achieved by restricting vitamin A in the food fed to commercial cows. In fact, by depleting liver stores and restricting the content in food, the grade of meat and percentage of intramuscular (IM) fat increase quite substantially. Better yield for livestock owners. Higher levels of blood glucose (BG) are also associated with lower vitamin A status and higher marbling.

HHHhhmmm... why??

Is the livestock which is raised commercially on grains clinically obese, diabetic, inflamed, cancerous (well, unlikely...they're slaughtered too young), high in MUFA, low in saturated fats, vitamin A and vitamin D deficient? With vast desaturase deficiencies?

Livestock owners may be purposefully inducing vitamin A deficiency in order produce higher USDA grade meat for the market. Should we be consuming this kind of low-quality protein?

Humans are actually not that different biochemically and physiologically from our bovine cousins. At one time, bovine insulin was used in Type 1 diabetes mellitus treatment and management. Until human recombinant insulin was developed, pork and beef-derived products were it. Porcine (pork) insulin actually produces less skin irritation and injection site adverse effects like (lipodystrophy, allergic reactions) than bovine, yet bovine filled the needs of many Type 1 diabetes individuals for decades.

One the most curious observations is how cows become very lean (and thus less profitable for ranchers) during spring and summer. This is theorized to be secondary to the increased vitamin A intake from pasturing and eating grass. Vitamin D and increased sunshine probably can be attributed to this relevation as well.

The last set of researchers link how our steroid nuclear receptors are all interrelated in controlling adiposity and the creation of fat cells (adipocytes). They propose a "model of vitamins A and D as suppressors on adipocyte development through retinoid/thyroid/vitamin D/fatty acid-activated/peroxisomal proliferator-activated receptor's subfamily." PPARs have been discussed here before and their crucial role in attenuating chronic and acute diseases including CAD and cancer: Happy Cows...etc.


Who might be vitamin A deficient?
--those who don't consume a lot of wild seafood/grassfed meat (like me but I've discovered... Whole Wallet now)
--those with Hashimoto's hypothyroidism -- Hashimoto's (vitamin A supplementation improves iodine efficacy; hypothyroidism=first sign of vitamin A deficiency in chicks)
--Oprah Winfrey
--Steve Jobs
--those with other autoimmune diseases: Grave's, RA, SLE, Sjogrens, multiple sclerosis, NASH, primary biliary cirrhosis, (??!) CAD, etc
--those with cancer -- see HERE and HERE and HERE--chronically ill
--those with infections or high CRP -- see HERE, HERE and HERE
--children less than age 4 and women -- see HERE too
--those who eat 'low fat'
--those with skin conditions (again, autoimmune origin and wheat-triggered): eczema, rosacea, skin cancer, poor wound healing, atopic dermatitis, psoriasis, dermatitis herpetiformis, porphyria cutaneous tarda
--diabetic-induced rats fed vitamin A deficient lab chow
--those with gluten enteropathy, (known v. unknown) wheat/casein allergies, 'leaky gut' and a poor intestinal barrier which prevent absorption of fat and fat-soluble vitamins
--those without a gallbladder who may not produce sufficient digestive enzymes to absorb fat and fat-soluble vitamins
--those who take Orlistat/Xenical or OTC Alli (weight loss pills which block fat and thus fat-soluble vitamins ADEK1 K2)
--those on antiseizure drugs (valproic acid, carbamezepine, phenytoin which increase metabolism/elimination of vitamin A)
--vegans
--those who have had gastric bypass which unnaturally cuts out a great portion of our most important absorptive surface area for fat and nutrients, the duodenum
--Inuit children with frequent lower respiratory tract infections and otitis media (who are probably no longer consuming their traditional H-G-fish Paleo diets but the S.A.D. grain-based one like Americans)
--third world countries where night-vision blindness is prevalent



What dose of Vitamin A is sufficient?

Like Vitamin D, we need adequate amounts Vitamin A for optimal health -- the desired amount is dependent on various factors: inflammation, growth, reproductive state, hormone state, etc. Vitamin A is not the same as beta-carotene, which is the precursor of Vitamin A. Beta-carotene is the common form found in multi-vitamins.

The current RDA for Vitamin A is 5,000 to 10,000 IU daily (take in AM -- may cause insomnia). Converting from RE mcg to IU see HERE.

Here are other benefits of Vitamin A discussed here: Synergy of Vitamin D and Its Co-factor Vitamin A
Consideration for Vitamin A supplementation is necessary if diet (wild seafood, grassfed meat, organ meats) are insufficient to meet daily requirements.

Ck out Vitamin A...for your healthwise b-o-t-t-o-m . . . line. I'll be watching it for you. *wink*

Hey Gibby -- this post is per your request!




CLICK ON CITATION TO VIEW (below)
"...long vitamin A restriction (LR) specifically increased fat deposition in the i.m. depot, without promoting an increase in the overall fatness of the animal. We conclude that feeding low-vitamin A diets may be a feasible and economical strategy to affect the site of fat deposition within the beef carcass. Pyatt and Berger (2005) hypothesized that the observed
seasonal decline in carcass grade during the fall may be associated with previous high-vitamin A intake during spring and summer. Additionally, typical feedlot diets are formulated to provide 2 to 3 times NRC (1996) vitamin A recommendations (Galyean and Gleghorn, 2002). Thus, feedlot cattle in the United States are fed vitamin A in excess of their requirements. Results of
this experiment provide evidence that the vitamin A level of the diet affects the site of fat deposition in feedlot cattle.

We recently reported that feeding low-vitamin A diets to beef steers appears to increase adipocyte differentiation in the i.m. depot without affecting s.c. adipocytes. This was accompanied by numerical in- creases in marbling scores and USDA carcass quality grades, with no effects on backfat deposition and USDA yield grades (YG; Gorocica-Buenfil et al., 2007). Marbling scores also were increased when low-vitamin A diets were fed to Japanese Black cattle (Adachi et al., 1999). The duration of vitamin A restriction required to improve i.m. fat deposition remains unknown. It is likely that to affect the vitamin A status of the animal, hepatic vitamin A stores need to be depleted. However, research in this area is negligible.

The effect of feeding low-vitamin A diets on beef fatty acid composition remains unclear. The enzymatic activity of stearoyl coA desaturase (SCD), required for the endogenous synthesis of CLA in ruminants, may be reduced by retinol (Alam and Alam, 1985). However, a numerical trend (P > 0.10) was observed in marbling score and the percentage of carcasses grading USDA Choice or above (from 28% in control to 50% in LR steers). If this effect were real, it would be economically important because most formulas used in the market to determine carcass value include a premium for
carcasses ≥ Cho (USDA Agricultural Marketing Service, 2006). The numerical increase in the percentage of highly marbled carcasses is in agreement with our previous experiment (Gorocica-Buenfil et al., 2007) where we reported a 7% increase in the marbling scores when low-vitamin A diets were fed to Angus-based steers."
Effect of dietary vitamin A restriction on marbling and conjugated linoleic acid content in Holstein steers. (PDF) Loerch SC et al. J Anim Sci. 2007 Sep;85(9):2243-55.Relationship between serum biochemical values and marbling scores in Japanese Black steers. Ohwada K et al. J Vet Med Sci. 1999 Aug;61(8):961-4.



"Slight changes in the fatty acid profile of s.c. fat of the steers were detected. A greater proportion of MUFA (LOW = 41.7 vs. HIGH = 39.9%, P = 0.03) and fewer SFA (LOW = 47.1 vs. 48.7, P = 0.03) were observed in vitamin A-restricted steers. This suggests that vitamin A restriction may affect the activity of desaturase enzyme (desaturase activity index, LOW = 46.9 vs. HIGH = 44.9, P = 0.01)."
Effect of vitamin A restriction on carcass characteristics and immune status of beef steers. Loerch SC et al. J Anim Sci. 2008 Jul;86(7):1609-16.


"It is well documented that grain feeding stimulates adipogenesis in beef cattle, whereas pasture feeding depresses the development of adipose tissues, including intramuscular (i.m.) adipose tissue. Additionally, production practices that depress adipocyte differentiation also limit the synthesis of monounsaturated fatty acids (MUFA). Marbling scores and MUFA increase in parallel, indicating that stearoyl-CoA desaturase (SCD) gene expression is closely associated with and(or) necessary for differentiation of marbling adipocytes. Similarly, marbling scores and fatty acid indices of SCD activity are depressed in response to dietary vitamin A restriction. In bovine preadipocytes, vitamins A and D both decrease glycerol-3-phosphate dehydrogenase (GPDH) activity, an index of adipocyte differentiation..."Cellular regulation of bovine intramuscular adipose tissue development and composition. Sawyer JE et al. J Anim Sci. 2008 Nov 7.



"The study aimed to systematically examine the effects of fat soluble vitamins and their analogs on terminal differentiation of adipocytes on the cellular and molecular aspects. It is well known that fat soluble vitamins especially vitamins A and D inhibit the differentiation of adipocytes in cultured cells. Furthermore, it has been revealed that the low level of dietary fat soluble vitamins, especially vitamin A and carotenoid actively stimulate the development of adipose tissue, namely bovine marbling in vivo. We have shown that the expression of retinoic acid receptor (RAR) alpha and gamma, retinoid X receptor (RXR) alpha and beta, and vitamin D receptor (VDR) mRNA were abundant in rat adipose tissue and 3T3-L1 cells. The autoregulated amplification and reduction of RAR, RXR and VDR mRNA by their own ligands, were observed in 3T3-L1 cells. Finally, we proposed the model of vitamins A and D as suppressors on adipocyte development through retinoid/thyroid/vitamin D/fatty acid-activated/peroxisomal proliferator-activated receptor's subfamily."
The possibility of active form of vitamins A and D as suppressors on adipocyte development via ligand-dependent transcriptional regulators. Sugimoto E et al. Int J Obes Relat Metab Disord. 1996 Mar;20 Suppl 3:S52-7. Review.

Saturday, January 17, 2009

Hormonal Imbalances: Oprah, Steve Jobs




Hashimoto's Hypothyroidism and Oprah Winfrey

I love Oprah. My sister 'M' loves Oprah. It would be a gigantic understatement to say that all my girlfriends and co-workers love Oprah.

Now, with that said, I feel extremely, deeply saddened when I see the most well connected woman and influential/popular educator sooooo disconnected with her health and hormones. Have you been there? Unable to control your body or weight? Like a typical Oprah nut, I spent a few nights madly emailing her about year ago in Jan 2008 about vitamin D and weight loss and optimal health (and my 50# weight loss story). Where did it go? Filed in the big phat Oprah-empire round file??


Who has not been in her precise shoes?

Read about Oprah's Thyroid Club HERE (NY Times).

Hashimoto's hypothyroidism is one of the most common female (and male) afflictions of the late 20th and 21st centuries. Nearly every one of my diabetes patients has Hashimoto's.

Why??

Why are 45+ million Americans burning their Thyroid to a toast, like Oprah?

In my 20's -- stressed, eating dorm food, trying do everything 'right', instead of gaining the freshman 'fifteen', I gained F-O-R-T-Y lbs (b/c... hey... can you say overachiever?).
[Another college curiosity was observing how my hormones/ cycles/ periods became imperceptibly and immutably N*SYNC with my female dorm-mates. Mense shifts are apparently secondary to pineal gland and pheromones (link and other refs from an astute friend, thanxxx dude). Recall, pheromones are picked up by the nose- vomeronasal system and subsequent hypothalamus/limbic brain (paleopallium).]


What was going on with that college weight gain, mood fluctuations, difficult concentrating, sluggishness, coarse hair/skin, skin tag growth/insulin resistance, cold intolerance, resistance to weight loss/exercise, high cholesterol, mental fog and general feeling of clinical cr*ppiness??

I wish I knew back then...



Oprah... let's try to clue you in, my honeybun... from my sad life lessons.

For me, in hindsight, there were a few situations that may parallel Oprah's, that are backed up by the medical literature that cause thyroid dysfunction.



How to Give Yourself Hashimoto's Thyroiditis 101:

--lack of sunlight/vitamin D/indoor habitation
--mental stress
--more mental stress
--sleep deprivation... (excessive mochas/lattes at Berkeley cafes)
--excessive 'social' calendar
--inherent family history of autoimmune disorders (who doesn't??)
--wheat, wheat, and more wheat ingestion ('comfort foods' craved in times of high cortisol/stress, right? how did I know the carbs were killing me?)
--lack of nutritious food containing EPA DHA, vitamin A, sat fats, minerals, iodine, etc
--lack of play, exercise, movement (or ?overtraining perhaps for Oprah's case)
--weight gain -- which begins an endless self-perpetuating vicous cycle of all the above (Is it stressful to balloon out for no apparent reason? YES)





Of course, it turns out there is a hheeeyyuuggee link between sunlight/vit D/melatonin and the neuroendocrine system.



These four research groups below discuss how our Hypothalamus-Pituitary-Thyroid-Gonad Axis is tightly affected by melatonin, Thyroid Hormones, neuropeptides like brain tachykinins, and our reproductive sex steroids (Estrogen and Testosterone).


Melatonin influences on the neuroendocrine-reproductive axis.
Díaz López B, Díaz Rodríguez E, Urquijo C, Fernández Alvarez C. Ann N Y Acad Sci. 2005 Dec;1057:337-64.
The neuroendocrine-reproductive axis designates the functional activity of the hypothalamus-pituitary-gonadal axis. A delicate synchronization of many inputs at these three different levels is vital for normal reproductive function. From the median basal hypothalamus, the median eminence releases gonadotrophin releasing hormone into the portal circulation to reach the anterior pituitary gland.


Evidence for pineal gland modulation of the neuroendocrine-thyroid axis.
Vriend J. Neuroendocrinology. 1983;36(1):68-78.
Although melatonin administration has been reported to inhibit blood T4 levels in both rats and hamsters, under certain experimental conditions melatonin administration can be demonstrated to have a counter-antithyrotrophic effect resulting in increased blood levels of T4 and thyrotrophin... The effects of melatonin on the neuroendocrine-thyroid axis are similar to its effects on the neuroendocrine-gonadal axis, leading to the hypothesis of a common site of action for the thyroid and gonadal effects of melatonin.


Modulation of the hypothalamo-pituitary-gonadal axis and the pineal gland by neurokinin A, neuropeptide K and neuropeptide gamma.
Debeljuk L, Lasaga M. Peptides. 1999;20(2):285-99.
Tachykinin concentrations in the hypothalamus and pituitary are regulated by steroid hormones. In the hypothalamus, estrogens and testosterone increase tachykinin concentration. In the anterior pituitary gland, estradiol and thyroid hormones markedly depress tachykinin concentrations.



REVIEW. Melatonin and the thyroid gland.
Lewinski A, Karbownik M. Neuro Endocrinol Lett. 2002 Apr;23 Suppl 1:73-8.
The confirmation of these relations in clinical studies in humans meets numerous difficulties, resulting - among others - from the fact that, nowadays, human beings, as well as certain animal species, used in experimental studies, have been living far away from their natural and original habitat. It makes almost impossible to compare the results obtained in particular studies performed in different species, on the pineal-thyroid interrelationship.
(Yes...we may be jacking up our hormones with artificial light, computer screens and TV.)




Oprah Likely Needs Vitamin D

Vitamin D ties everything together. The above two pictures come from the below research article (Sunlight--can it prevent as well as cause cancer?). The authors review: "The active form, 1.25D,, is a full member of the endocrine system, and as such interacts with virtually every organ in the body (31, 32). Especially noteworthy is its interaction with the sex and pituitary hormones (32-34), e.g.,the promotion of l-a-hydroxylation of 25D, by prolactin (34), since some of these interactions provide a mechanism for participation of 1.25D, in the control of cell growth in the reproductive organs . . . The Darwinian view of evolution suggests that loss of body hair in Homo sapiens should have some survival advantage, and it is difficult to think of reasons other than that this provides ready access of sunlight to the skin . . . lack of sufficient sunlight contributes to the known high incidence of carcinoma of the prostate in black American men and to the more aggressive progression of carcinoma of the breast in black women."



Vitamin D interacts with all the steroid nuclear receptors especially Thyroid Receptors and Vitamin A/Carotenoid Receptors (The concept of multiple vitamin D signaling pathways. Carlberg C. J Investig Dermatol Symp Proc. 1996 Apr;1(1):10-4.)

Oprah has a few risk factors for low blood vitamin D:
--stress -- our body burns up Vitamin D to maintain cellular processes under stress and infections
--wheat consumption (Stephan discusses this very well: Vitamin D and Celiac/Gluten Sensitivity) (and ?leaky gut prevent absorption of fat soluble vitamins)
--pigmented skin
--indoor lifestyle
--makeup/sunscreen
--living north of the 37th latitude where UVB solar radiation (the activating wavelength for vitamin D) is scarce for 40-50% of the calendar year
--age


Unless Oprah is receiving bio-identical hormone replacement, then her natural steroid sex hormones are likely to be 'off' and this would affect her Thyroid as well. Women from age 35 yo and up start experiencing declines in sex hormone due to the atresia (dissolving) of the eggs in the ovaries, one of the main sources of Estrogen and Testosterone. After Menopause (average age: 51 yo), nearly all the eggs are gone. Again, as the above emphasizes, the lack of significant sex hormones will profoundly affect the Hypothalamus-Pituitary-Thyroid glands.



What can help Oprah's Thyroid and take her to optimal health?
--Richard, at Free the Animal Oprah's Recipe For Failure -- And My Solution For Success, started this conversation and many of his fans chimed in.
--Scott Miller wrote:

"Here are ten quick mistakes I see her making that will sabatoge her efforts:
[1] Eating starches and grains.

[2] Eating low fat foods (like the egg whites rather than full eggs)
[3] Eating too often...How many omnivores in nature eat five times per day, regularly, like clockwork?
[4] Using fat-free dressings.
[5] A stunning lack of variety in salad-type vegetables (pretty much always romaine lettuce).
[6] Having a killer temptation like those blue chips in the house.
[7] Stead-pace aerobics violate the power law of human conditioning.
[8] And doing aerobics too often.
[9] Slow-twitch-fiber-only strength training.
[10] Strength training too often. "


Besides the paleolithic lifestyle, Oprah could use some natural neolithic bio-identical hormone replacement, starting with the big 'D':
--Vitamin D to blood [25(OH)D = 70 ng/ml] which will probably require about 8000 IU daily in the morning (Cannell doses 1000 IU per 25 lbs -- Oprah reports weight is ~200 lbs)
--Cortisol Reduction -- rest, relaxation, meditation, turn off the Crackberry
--Correct hGH Deficiency-- eat enough fat/protein, carb restrict, sleep well and enough, induce some strain/pain/gain on the muscles, food deprivation 18-36 hr 2-3x/wk
--Correct excess insulin -- stop wheat
--THYROID Replacement-- correct gradually to tolerance and mood, energy, cognition (Dr. Davis goal TSH: 1.0; Free T3: upper nl)
--Estrogen (estriol E3 primarily) -- restore to personal youthful levels prior to peri- and menopausal changes; provides cognition (our brains are FULL of estrogen-receptors), mentation/memory, skin/hair/mucuous membrane functioning, immunity, etc
--Natural Progesterone -- calms and restores all the other cycles (Avoid Provera, Levonorgestrol, which are progestins, man-made, associated with cancer and lower HDL 20-30%)
--Testosterone -- yes women need this just like men... provides confidence, vitality, well-being, affiliation, motivation, zest, in addition to libido
--DHEA-S
--Melatonin





How to Stop the Autoimmune Process of Hashimoto's

When one of our organs is jacked how do we recover it? Can we induce our immune system to heal and restore function? Certainly! With time, appropriate nutrients and stimulus, I believe depending on the extent of the incurred damage, our bodies have the capacity to regenerate itself. With Vitamin D repletion and Wheat-Cessation, I have observed a trend of improved TSH (including my own from 1.3-1.9 to 1.0 when my 25(OH)D stays above 60 ng/ml). Why? Vitamin D interacts intimately with thyroid, vitamin A/carenoid and other steroid hormone controls, including the sex hormones.

These below nutrients and lifestyle changes have been shown to aid the Thyroid to heal and restore functionality:
-stopping wheat which triggers our immune systems: innate+humoral
-stopping wheat which triggers genetic expression of stress responses
-stopping wheat which results in rapid rises of insulin
-stopping gluten/wheat/barley/rye
-stopping beans, peanuts, legumes (lectins)
-stopping dairy (which contain opioid-like proteins like wheat)
-stopping grains (rice, corn, etc) -- which are all grass-derived (*ha * I didn't say WEEDS but that's what I mean)
-proper nutrients which are the building-blocks of the Thyroid Gland and Thyroid Enzymes: proteins (taurine, leucine, arginine, OKG, L-carnitine, etc), minerals (IODINE, Mg, Zn, Se, Chromium, Bo, etc)
-B-vitamins (including α-lipoic acid)
-Vitamin D3 (goal 25(OH)D=70 ng/ml)
-Vitamin E (tocopherols, tocotrienols)
-Vitamin K1 K2
-Vitamin A
-Carotenoids (grassfed meat, wild seafood, Krill oil/Astaxanthin)
-EPA + DHA (ditto) -- high dose if extreme inflammation is present
-Antioxidants (Flavonoids, CoQ10, ALCAR/α-LA, Pycnogenol, etc)
-Avoid dietary and environmental toxins (nitrite preservatives, plastic, petroleum, bisphenol, heavy metals (Lead, Mercury), endocrine disrupters, pesticides, dioxins, etc)





Hashimoto's Thyroiditis Related to Autoimmune Genes

All autoimmune conditions are related to differences in our immune system. Even Migraines are associated with a certain type of immunity variation (Prevalence of HLA DQB1*0602 allele in patients with migraine). Hashimoto's is strongly tied to HLA DR5 types, vitamin D receptor anomalies, and CYP1 alpha hydroxylase (vitamin D activation enzyme) variations. It turns out also that Addison's Disease is tied to the same Cyp enzyme variant or what is known as a polymorphism.
A promoter polymorphism of the CYP27B1 gene is associated with Addison's disease, Hashimoto's thyroiditis, Graves' disease and type 1 diabetes mellitus in Germans.
Association of vitamin D receptor gene 3'-variants with Hashimoto's thyroiditis in the Croatian population.
Vitamin D receptor gene polymorphisms are associated with risk of Hashimoto's thyroiditis in Chinese patients in Taiwan.
Vitamin D receptor genotype is associated with Addison's disease.
Vitamin D 1alpha-hydroxylase (CYP1alpha) polymorphism in Graves' disease, Hashimoto's thyroiditis and type 1 diabetes mellitus.
Vitamin D receptor gene polymorphisms in Hashimoto's thyroiditis.
[Genetic markers in thyroid autoimmune diseases]





Steve Jobs: Addison's Disease?

Via Apple headquarters, Mr. Jobs issued a statement reporting that he was receiving treatment for 'protein wasting' for what doctors believed was caused by a 'hormonal imbalance.' He states he does not have cancer. Could Mr. Jobs be suffering from the same ailment as our late great president John F Kennedy? Mr. Jobs was reported to consume a vegetarian diet which are often devoid of EPA and DHA -- protectors against autoimmune disease as well as pancreatic cancer (see below). EPA and DHA are long chain omega-3 polyunsaturated fatty acids (PUFA) which ONLY come from animal sources. EPA and DHA are like Comcast and DSL -- they provide the reliable high-spped connections for electronic conductions in our nervous systems (compare v. lame lowtech modem/omega-6). Our brain is comprised of inordinate amounts of DHA and EPA. Every cell membrane. Unfortunately humans do not induce enough of the enyzmes to convert vegetarian omega-3 ALA to EPA + DHA in our bodies. If you are not stressed, then it is unlikely to matter. ALA from vegetarian sources would sufficiently maintain health. Most people however undergo some degree of stress or oxidative damage from daily living (like...umm...breathing or... hard breathing at Crossfit or HIIT). Although Mr. Jobs apparently did not have the most aggressive form of pancreatic cancer, he had surgery a few years ago for a neuroendocrine tumor in the pancreas. Addison's may also originate from metastatic tumors to the adrenal glands.

Has Mr. Jobs been under stress? Maybe...
(1) Cancer survivor
(2) Rolled out the best neolithic tech advances of our times: iPOD, iPHONE
(3) Apple innovator/revivor/evolver

o Modulatory effects of EPA and DHA on proliferation and apoptosis of pancreatic cancer cells.
o Omega-3 fatty acids improve liver and pancreas function in postoperative cancer patients.
o Fish oil and treatment of cancer cachexia.




Do you want Pancreatic Cancer??

Consume a lotta Omega-6 refined veggie oils like Sunflower or Safflower oil
and/or develop Omega-3 Deficiency
and/or eat a lot of Fructose
and/or a USDA Whole Grain Diet:
Opposing effects of n-6 and n-3 polyunsaturated fatty acids on pancreatic cancer growth.
Effect of dietary omega-3 and omega-6 fatty acids on development of azaserine-induced preneoplastic lesions in rat pancreas.
Carcinogen-induced lesions in the rat pancreas: effects of varying levels of essential fatty acid.
Effect of dietary intake of fish oil and fish protein on the development of L-azaserine-induced preneoplastic lesions in the rat pancreas.
Dietary glycemic load, added sugars, and carbohydrates as risk factors for pancreatic cancer: the Multiethnic Cohort Study.

Dietary sugar, glycemic load, and pancreatic cancer risk in a prospective study.
Etiology of nonresponsive celiac disease: results of a systematic approach.
Aldolase C in neuroendocrine tumors: an immunohistochemical study.
Dietary fructose enhances the development of atypical acinar cell nodules in the pancreas of rats pretreated with N-nitrosomorpholine.




Hormone Imbalances and Organ Failure

Like Oprah, several hormonal imbalances can lead to organ failure due to an autoimmune process. In Addison's, the organ mainly affected is the adrenal glands which provide Cortisol and other cholesterol-derived hormones to the body. Without a minimal amount of Cortisol, we do not make muscles or store fat. Addison's leads to muscle wasting, weight loss, dizziness, and depression. Excessive Cortisol, on the other hand, causes a condition known as Cushing's where excessive abdominal weight gain, moon-face, thin-skin, muscle wasting, fatigue and insomnia occur.



Other Thyroid Sources:



Hormone Balancing Resources:

  • Dr. Uzzi Reiss, MD OBGYN: Natural Hormone Balance
  • Dr. Michael Colgan, PhD: Hormonal Health -- Nutritional & Hormonal Strategies for Emotional Well-Being & Intellectual Longevity
  • Colgan, The Sports Nutrition Guide
  • Dr.Cheryle Hart, MD OBGYN: Hormones By Hart