Wheat: Raises Insulin and Upregulates 'Bad' Genes

Ancient Wheat: 'Gladiator '
'Now We Are Free' Hans Zimmer, Lisa Gerrard

Can our food alter gene expression?

Absolutely so!

As Hippocrates once said, 'Let food by thy Medicine... and Medicine thy Food.' I'm sure he didn't mean medications as they exist now as chemicals or benzene rings (derived from petroleum) mass synthesized in factories for global consumption. The below FUNGENUT study recently showed the importance of how different sources of carbohydrate containing foods immediately changes gene expression in our favorite organ -- the omentum -- the stubborn fat lying on our bellies -- yes, the one covering up your those fabulous 6-pack abs. (Diagram: Ludwig, D. (2002) JAMA )

In a small group of subjects, 2 diets (Rye-Pasta -- mildly lower in GI; Oat-Wheat-Potato -- high GI carbs) were compared for 3 months. At the end no change in weight or insulin resistance, insulin levels, or glucose concentrations occurred. The profile for insulin (1st phase) secretion mildly improved in the Rye-Pasta group.

Interestingly, other than showing that wheat sucks (and perhaps oat and potato) gene expression was entirely affected by simple changes in carbohydrate content and the Glycemic Index (GI measures how long and how fast glucose enters the blood stream after consumption). Rye (endosperm) bread has a GI (glycemic index) of approximately 60-70. Pasta's GI is about 60-70 as well (depending on the type and how al dente/not-overcooked).

Wheat bread on the other hand is about 90-100 (close to pure glucose). Oats about 70 and potatoes 80-100 (without cream or butter which slows the uptake of starches into the stomach blood circulation which would effectively lower the GI). American Russet potato even exceeds glucose, 110 (!wow).

CARBOHYDRATE COMPOSITION OF FOOD PROVIDE MOLECULAR EFFECTS AND LOW-GI CARBS DOWNREGULATE 'BAD' GENES:

"Prior microarray studies found differences in gene expression between overweight and lean individuals (2) and after energy restriction (3); however, changes in the ratio of fat to carbohydrate did not alter gene expression (3). The study by Kallio et al makes a significant contribution to the literature by demonstrating the potentially major effects of dietary composition on gene regulation, independent of energy intake and body weight. Two specific findings concerning the low-insulin-response diet merit particular attention: the down-regulation of both hormone-sensitive lipase (HSL) and TCF7L2. "

"HSL, a key enzyme in the release of fatty acids from adipose tissue, has been proposed to affect body weight and metabolic variables. Mice made deficient in HSL by genetic manipulation are resistant to genetic- or diet-induced obesity (4, 5). Women carrying an allele associated with decreased HSL activity have lower fasting and simulated insulin concentrations, and men with this allele have lower nonesterified fatty acid concentrations (6)..."

"The transcription factor TCF7L2 is the strongest known genetic predictor of type 2 diabetes. A microsatellite within intron 3 of this transcription factor occurs with increased frequency in individuals with type 2 diabetes, which corresponds to an estimated population attributable risk of 21% (7)..."

"The present study (BELOW) has direct implications concerning our understanding of the dietary glycemic index (GI). The GI is a system for classifying carbohydrate-containing foods according to how blood glucose concentrations change in the postprandial period (reviewed in reference 8). High-GI meals produce greater postprandial insulin concentrations and C-peptide excretion than do nutrient-controlled low-GI meals. Observational and interventional studies have linked GI to the risk of obesity, diabetes, heart disease, and cancer, although the topic remains much debated. One factor contributing to this ongoing controversy is the relative paucity of data regarding the relevant molecular mechanisms. If differences in insulin secretion mediate the genetic effects observed by Kallio et al, similar effects would be expected to occur with both low-GI and high-GI diets. This possibility is supported by a human study and several rodent studies, which showed potentially beneficial changes in the expression of HSL and other relevant genes with a low-GI diet (8, 9)."

Contrastingly, the high-GI wheat (+oat+potato) diet upregulated 62 genes including those associated with activation of DEATH GENES:
-- Stress
-- Oxidative damage
-- Impaired immunity

So... high carb diet translates to... the equivalence of a STRESS RESPONSE. The authors discuss in more depth the results from the FUNGENUT Study..."Interestingly, the 12-wk oat-wheat-potato diet seemed to especially activate genes responding to stress. The oxidative stress pathway, interleukin pathway, and inflammation mediated by the chemokine and cytokine signaling pathway were also activated. Moreover, the present data suggest that the oat-wheat-potato diet, which induced repeated high insulin responses, can provoke alterations in immune status and inflammation. It is well established that adipose tissue has a role in inflammation (39). Cross-sectional epidemiologic data suggest that whole grains and a low-glycemic-index diet may reduce systemic inflammation in women with T2DM (40). Up-regulation of gene expression for serum and glucocorticoid-regulated kinase suggests activation of the glucocorticoid axis, which can occur in response to various stress stimuli (cytokines, aldosterone, growth factors, oxidative stress, heat shock protein activation, and glucocorticoids) (41). Activation of the pituitary-adrenal glucocorticoid axis may be involved in the pathogenesis of the metabolic syndrome (42)."

Dietary carbohydrate modification induces alterations in gene expression in abdominal subcutaneous adipose tissue in persons with the metabolic syndrome: the FUNGENUT Study.
Kallio P, et al. Am J Clin Nutr. 2007 May;85(5):1169-70.
Department of Clinical Nutrition, Food and Health Research Centre, University of Kuopio, Kuopio, Finland.
BACKGROUND: Diets rich in whole-grain cereals and foods with a low glycemic index may protect against type 2 diabetes, but the underlying molecular mechanisms are unknown.
OBJECTIVE: The main objective was to test whether 2 different carbohydrate modifications--a rye-pasta diet characterized by a low postprandial insulin response and an oat-wheat-potato diet characterized by a high postprandial insulin response--affect gene expression in subcutaneous adipose tissue (SAT) in persons with the metabolic syndrome.
DESIGN: We assessed the effect of carbohydrate modification on SAT gene expression in 47 subjects [24 men and 23 women with a mean (+/-SD) age of 55 +/- 6 y] with the features of the metabolic syndrome in a parallel study design. The subjects had a mean (+/-SD) body mass index (kg/m(2)) of 32.1 +/- 3.8 and a 2-h plasma glucose concentration of 8.0 +/- 2.3 mmol/L. Adipose tissue biopsies were performed, and oral-glucose-tolerance tests and other biochemical measurements were conducted before and after the intervention.
RESULTS: We detected 71 down-regulated genes in the rye-pasta group, including genes linked to insulin signaling and apoptosis. In contrast, the 12-wk oat-wheat-potato diet up-regulated 62 genes related to stress, cytokine-chemokine-mediated immunity, and the interleukin pathway. The insulinogenic index improved after the rye-pasta diet (P=0.004) but not after the oat-wheat-potato diet. Body weight was unchanged in both groups.
CONCLUSIONS: Dietary carbohydrate modification with rye and pasta or oat, wheat, and potato differentially modulates the gene expression profile in abdominal subcutaneous adipose tissue, even in the absence of weight loss.
PMID: 17490981

These wonderful graphs from Finland researchers illustrate how the toxic effects of grain sources of carbohydrates occur when wheat and rye are fed to healthy volunteers. Above a glucose blood concentration of 150 mg/dl (=8.3 mmol/L), glucose starts to cause changes in protein folding and glycosylating proteins and tissues. Diabetes micro-vascular complications like eye/kidney/nerve ending damage are related to toxic concentrations of glucose. Imagine sugar coating the organs over time. The higher the concentration, the longer the duration, the more thicker and more damaging the sugar coating. Insulin is controlled by several factors. Food is one of the most potent controllers, with carbohydrates and their respective GIs raising insulin levels the most. Excessive insulin induces inflammation, which can progress and cause arterial stiffness, high blood pressure, Metabolic Syndrome, obesity, and also heart disease. Longevity has been associated with lower insulin levels. The below trial demonstrates the direct relationship in 18-year old men between fasting insulin and the existence of cardiovascular markers. The curves for low or no GI foods have no peaks and in comparison are relatively flat. Without a surge in insulin, inflammation is kept at bay.

Foods with no or little GI:
-- Non-starchy vegetables
-- Protein (tofu, meat, fish, etc)
-- Monounsaturated fat
-- Omega-3 PUFA
-- Saturated fat

The goal for an optimzed health status for nearly all metabolic and cardiovascular goals is NORMAL. Therefore the optimal range for insulin is as low as possible less than 5 - 10 mIU/L. The goal for glucoses pre-meal is less than 83 (=4.6mmol/L) and after meals less than 110 to 120 (=6.1 to 6.67mmol/L).

Relationship between fasting insulin and cardiovascular risk factors is already present in young men: the Verona Young Men Atherosclerosis Risk Factors Study.
Bonora E, et al. Eur J Clin Invest. 1997 Mar;27(3):248-54.
The associations between fasting plasma insulin concentration and risk factors for cardiovascular disease were examined in 979 18-year-old men participating in the Verona Young Men Atherosclerosis Risk Factors Study, a cross-sectional population-based study. Body mass index (BMI), waist-to-hip ratio (WHR), plasma triglycerides and uric acid concentrations, and blood pressure values significantly increased, and the high-density lipoprotein (HDL)-total cholesterol ratio decreased, across quartiles of fasting insulin. Total and low-density lipoprotein cholesterol, concentrations did not change significantly with the increase in fasting insulin levels. After adjustment for BMI, WHR, smoking, alcohol intake and physical activity, only plasma triglycerides significantly increased across insulin quartiles (F = 7.1; P less than 0.001). However, systolic blood pressure and uric acid were close to statistical significance (P = 0.06-0.07). Multiple linear regression analysis confirmed that plasma insulin was independently correlated with plasma triglycerides and, to a lesser extent, with blood pressure and uric acid concentration. This analysis pointed out that BMI was a stronger independent predictor of all cardiovascular disease risk factors than fasting insulin. When subjects were categorized according to the number of metabolic and haemodynamic disorders occurring within the same individual, subjects with multiple disorders (i.e, three or four) had higher plasma insulin levels than those with none or few disorders, even after adjusting for BMI, WHR and behavioural variables (F = 4.0; P less than 0.01). These results indicate that hyperinsulinaemia is already associated with a cluster of cardiovascular disease risk factors in young adulthood, the strongest independent association being with plasma triglycerides. PMID: 9088862

ONCE . . . People Stop Grains

It's not that h-a-r-d actually...

Many people I know give up g-r-**-**-n-s...

Who? Those at T-Y-P . . . those at Crossfit...reader's of this blog and others of the emerging HAWT new Paleo community...

Some of my faves:
Conditioning Research (Chris H., YOU R-O-C-K, ur #1)
Free the Animal (the 'other' transformed animal...who shares untainted fairy stories and delish food...uuummm...p**rn)
WholeHealthSource
Darwin's Table (transformation...more great food...uuummmm... p**rn)
Asclepius...Feed Your Mind, Grow Your Soul, Work Your Body (god of healing and medicine *luv that name*)
Open Water: Fitness…Science…Fun…Adventure
Hyperlipid hosted by Peter...brilliant THINCer
Matt Metzgar
(and... of course... many many others!!)



Paleo is so primally...sexy.

Quitting grains is not just Paleo -- it's the quickest way to a quality life!

What's the Paleo prescription?


Rx: Movement/play/slumber
Rx: Whole veggies, seafood/meat, good fats, seeds/nuts, minimal fruit; feed-feed/fast
Rx: Ancestral vitamin D and EPA DHA levels (Calcidiol [25(OH)D]=70 ng/ml; cod/fish oil to optimization of brain, 5 senses, muscle/heart function)



ONCE people stop grains (primarily wheat) they notice many changes and improvements. To say they undergo a restorative transformation is an understatement. Studies like the FUNGENUT show that wheat and high carb foods like white potatoes trigger a state of chaos and stressful derangements in our bodies (high insulin, high MMPs, high gene expression of 'death' genes).

The promotion of whole grains in the U.S. for 'wholesome' health is simply ridiculously whole cr**p (I'll try to keep it G-rated today *wink*).

Here is what happens when people stop those 'd*mn dirty grains'...Degree of improvement depends on degree of compliance with cessation of wheat... 6-12 months for perceptible permutations. Patience and persistence pays...


ONCE people stop grains...they're IBS (irritable bowel syndrome) eternally ends (essentially, cured of cramping/bloating/constipation) unless re-challenged

ONCE people stop grains...they report their aching knees stop knocking

ONCE people stop grains...their skin glows and radiates...no ACNE

ONCE people stop grains...I notice their waistline starts to emerge...how SEXY...many other things... uummm emerge too

ONCE people stop grains...WEIGHT LOSS BECOMES SUPERFLUOUS...easily attained 10 lbs per month

ONCE people stop grains...I notice their thoughts become thoughtful..lucid again

ONCE people stop grains...they can stop 200 units of insulin and/or other diabetes medications and/or their hypertensive medications and/or their gout medications

ONCE people stop grains...all report their skin tags fall off or stop appearing

ONCE people stop grains...the males' ED (erectile dysfunction) reverses...they're uummm... erected... well... sometimes... (Arg and Pycnogenol help greatly to speed this restoration up; see HERE and HERE)

ONCE people stop grains...their PSA (prostate antigen test) plummets (in parallel, Prostate Cancer risks reduce too)





ONCE in a Lifetime (Other link loves, courtesy of Youtube.com)
-----Version I: G-rated, Enigma-Gregorian
-----Version II: NAWT G-rated... nsfw...Princessa

Insulin and Aging: How Paleo Works

Ai M showed the disparity between insulin changes between oral glucose loading (75 grams glucose) versus a high saturated fat CREAM dosing.


Carb equivalents 75 grams = 5 servings CARBs

Go to nutritiondata.com for more comparisons.

1 serv CARB = 15 grams

Dairy -- 1 cup milk = ~15 g

Fruit -- 2 bites is about 15 grams (small palm-full).

Grains (~ 15 grams):
Oatbran 1/3 cup. Oatmeal 1/3 cup. Bread 1 slice or half-slice depending on the density. Rice 1/3 cup. Pasta 1/3 cup. Broccoli 2-3 cups just kidding but infinitely more compared with grains which have an insanely high-carb density as well as genetic propensity to trigger stress, glucocorticoid and the expression of other 'bad' genes. See prior animal pharm FUNGENUT post HERE.

Legumes (~15 grams):
1/2 cup beans


Ai M et al. Clinica Chimica Acta 387 (2008) 36–41. Email me for the PDF if desired.

What is PALEO?
None of the above
--no dairy (except casein-free clarified butter/GHEE or whey protein)
--no grains (corn, oats, gluten (wheat/barley/rye), rice, etc)
--no legumes (beans, soybeans (unlesss soaked+fermented), peanuts)


Please see recent NephroPal post:
Insulin and Aging: How Paleo Works

Click above link...

Major Demything...

XerXes
'Cell Progression'
Photography from a hot-air ballon by Yann Arthus-Bertrand

"With Earth from above, I simply want people to see the Earth as it is today, as faithfully as possible. What motivates me is the impact a photograph can make within the framework of environmental preservation. The great novelty of our time is that mankind has the power to change its environment and I want my photos to testify to this fact so people can realise this."

--Yann Arthus-Bertrand



Demything Myths in My Mind

A couple of things I harass and harp on are now shaded in grey instead of the archetypical black-white which I tend to prefer for simplicity and reductionism. My kids eat gluten (at school and parties) and in choosing my battles, I've accepted certain facts of life. They're going to be exposed, they like it and we just all have to do our best. And our best is a template based on strictly relative terms (e.g. my mood). Gluten is definitely a struggle stillsince it permeates all restaurant food and sauces. On alibaba.com, one can purchase cheap bags of high-protein (high-toxicity) hybridized modern wheat or maize gluten (vital wheat gluten 75% of total protein wet content) in which a restaurant, supplier or large-scale cook can 'doctor up' their goodies. Gluten imparts many favorable food benefits: moisure, 'perfect viscoelasticity', taste, addiction, bounciness, baked good fluffiness, sauce thickening, dough extension, sausage filler, meatball tenderness (lionhead casseroles are infamous), petfood 'protein', etc.

With all that said, since moving to Shanghai, quite honestly I have been surprised by the number of people aware of gluten intolerance and progressive in that manner, and grateful that the volume of gluten is far less here in China than the USDA-Big Agra-permeated culture of the U.S.

Anyway. Call me skeptical today...



Seven (Paleo) Myths that I've Slowly Come to Highly Suspect

1. Gluten is 100% bad and toxic
--Demyth: Not for everyone (especially if no intestinal permeability), every moment, every minute, every dose

2. Dairy is non-paleo
--COME ON. Human variance, intestinal permeability, status of DPP-IV (casein enzymes) and gut flora determine this. Same with gluten...

3. Intermittent fasting is 100% safe
--See prior adrenal tagged posts. Martin Berkham fanboys [I'm jealous of y'lls kevlar-coated adrenal glands] may go please very gently f*ck yourselves...and continue cortisol-inducing yo-yo dieting and eating cheesecake. Sorry. #FAILEO if one has f*cked up adrenals.

4. VLC/ketosis is 100% safe
--Demyth: see above

5. High glycemic index safe starches are 100% safe
--Demyth: high GI carbs can induce inflammatory cascades of gene expression. For who? See the FUNGENUT study. I dunno...

6. Low carb (less than 200 grams/day) or VLC/ketosis induces 100% fat loss
--Demyth: it depends on hormones and insulin sensitivity(primarily adrenal/NE/EPI and anabolic ones, progesterone and testosterone and if there is excessive E or xenoestrogens). See Ebbeling Ludwig et al JAMA 2007; side figure those who exhibit decent insulin sensitivity (maintain low insulin after 75 grams of lines of glucose) can lose weight on any kind of diet (this study used hypocaloric, low GI, 170 g v. 220 g carbs). IR=insulin resistance

7. High glycemic index safe starches (white stuff -- lines of dextrose, white rice, white modern potatoes, table sugar, etc) induce 100% optimal health and fat loss
--I'm ambivalent because I cannot and I know a lot people who this is the case. Why? Hormone fluxes are sometimes OFF and subOPTIMAL. Who loses fat and gains optimal health with higher glycemic loads and higher GI foods? I've seen this work well in the athletic, the insulin sensitive and the ones who perform high or decent volume glycolytic activity. See Poliquin on Carb Intake to Meet Glycolytic Repetition Volume. Also gotta see Sloth and Astrup.




What I Do Know

1. Modern wheat is SUPER TOXIC, SUPER ADDICTIVE, SUPER FATTENING, SUPER INFLAMMATORY

2. Modern wheat contains an estimated SEVERAL HUNDREDS-FOLD more (toxic) proteins than heirloom or non-hybridized wheat

3. The USDA is playing a joke on us... I don't trust the pyramid or anything else they purport, especially if it involves Monsatan or their former executives who now frequently staff places like the FDA or EPA (Environmental 'Protection' Agency). BRILLIANT.

4. If intestinal permeability exists, you'll be guaranteed suboptimal health, chronic sublethal infections and significant levels of cellular inflammation which may or may not ever be detectable by standards of non-integrative medicine

5. Pharmaceuticals generally do not work and in fact worsen. The worse pharmaceuticals cause long-range adverse effects on intestinal permeability and endogenous hormone fluxes (broad spectrum antibiotics, Z-paks, proton pump inhibitors, acid blockers, oral birth control, synthetic hormones, glucocorticoids, prednisone, etc)

6. Too much sugar is toxic, addictive, fattening and inflammatory. When I'm not stressed out and working out a ton, I can do sugar with relative impugnity. YET. During certain times of my menstrual cycle or when I am not strenuously working out, I notice if I hit (some) sugar (e.g. organic palm, organic coconut sugar, white stuff, etc) then I will inevitably want to do lines of crack/sugar over and over and over and over infinitum again (e.g. candy cigarettes or almond flour pound cake or cookies).

7. Everything makes horrorific sense in light of evolution

8. Bell shaped curves -- I like these; these typically represent well

9. I don't need RCTs to tell me the sky is blue or that something makes sense
(sometimes the ridiculousness in Pubmed makes me throw my hands up)

10. We're omni-whores, consumers of everything and we still survive



References

Live probiotic Bifidobacterium lactis bacteria inhibit the toxic effects induced by wheat gliadin in epithelial cell culture. K Lindfors,* T Blomqvist,* K Juuti-Uusitalo,* S Stenman,* J Venäläinen,† M Mäki,* and K Kaukinen‡. Clin Exp Immunol. 2008 June; 152(3): 552–558.

INFECTIONS, TOXIC CHEMICALS AND DIETARY PEPTIDES BINDING TO LYMPHOCYTE RECEPTORS AND TISSUE ENZYMES ARE MAJOR INSTIGATORS OF AUTOIMMUNITY IN AUTISM. A. VOJDANI,J.B. PANGBORN; E. VOJDANI; E.L. COOPER. INTERNATIONAL JOURNAL OF IMMUNOPATHOLOGY AND PHARMACOLOGY Vol. 16, no. 3, 189-199 (2003).

Low glycemic index diets and body weight. B Sloth and A Astrup. International Journal of Obesity (2006) 30, S47–S51.

Effects of a Low–Glycemic Load vs Low-Fat Diet in Obese Young Adults. Ebbeling, Ludwig, et al. JAMA. 2007;297(19):2092-2102. 297(19):2092-2102.

Evoke Tranquility...

J. L. Merlin
Evocacion

Courtesy of Youtube.com

Melatonin has been on my mind...ever since Dr. D got me turned on to it here a little while ago. I know several people who take it and TOTALLY swear by it for insomnia. How can this hormone have such far-reaching benefits and effects?

It's used for:
--jet lag
--inducing hGH secretion
--hypertension
--breast cancer prevention
--oxidative damage protection
--insomnia
--vasculature un-responsiveness (relaxation/constriction with ACh or adrenaline)
--migraine prevention
--modulation of behavior and sleep patterns in autistic children
--natural aromatase inhibitor -- prevents excessive conversion of Testosterone to Estradiol (E2) and Androstenedione to Estrone (excessive Estrone (E1) is not good -- 'storage' form of estrogen in our adipose tissues and linked to promotion of cancer...and ??perhaps heart disease?)

Melatonin also is the master hormone behind skin changes in amphibians and reptiles.

How about us humans? You know how teenagers get all moody and starting staying up late and waking up late? And how they may transform from sweet kids to stinky Twilight sulkiness? Melatonin drops as sexual maturation occurs and this may lead to disrupted sleep cycles. This researcher and author of the textbook Dev Bio notes that Melatonin is the suspected hormone that allows human metamorphosis to occur: "The various morphological and behavioral changes of puberty are due to the actions of these hormones on the various target tissues. As in metamorphosis, there appears to be a maturation-inhibiting hormone whose activity decreases to permit the reactivation of development. In humans, this hormone is probably MELATONIN, whose serum concentration decreases as that of LH rises (Waldhauser and Dietzel, 1985)."


So who may experience dysregulation of Melatonin? Which came first...the chicken or the egg? Dysregulation of the hypothalamus/pituitary/pineal axis with wheat-assaults, in utero maternal vitamin D deficiency and/or neonatal/developmental EPA-DHA deficiency?

Are we epigenetically pushing our species into extinction?

The medical literature shows that many types of individuals are deficient in melatonin in the diurnal secretion that normally occurs at night -- in the pitch black inkiness of the night as nature intended (of course unless the full moon is shining). Normally melatonin starts to rise at 7pm and peaks at 2am then gradually falls again by dawn. Seasonal rhythms obviously exist also. Anciently controlled tides that we may not even be conscious of. In Scotland, scientists have recently shown how "Melatonin acts directly on anterior-pituitary cells, and these then relay the photoperiodic message back into the hypothalamus to control neuroendocrine output...(to trigger increases in TSH which subsequently signals activation of T3 (active thyroid hormone from T4) for increased metabolism and reproduction)...In mammals this provides the missing link between the pineal melatonin signal and thyroid-dependent seasonal biology (Hazlerigg Curr Biol. 2008 Aug 5;18(15):1147-52).

--Autistic spectrum children -- they tend to also display a genetic polymorphism, a deletion for the gene encoding the last enzyme for the making of Melatonin
--Individuals with coronary artery disease
--Type 2 diabetes with cardiac autonomic neuropathy (stiff heart rate variability (HRV))
--Wernicke-Korsakoff syndrome -- ie, brain-damage due to malnourishment -- seen in gastric bypass and alcoholics
--Sleep deprived individuals, swing shift workers, travel involving time zone shifts
--Hyperthyroid, hypothyroid (higher melatonin secretion but also higher elimination in the urine found)
--Environmental lighting conditions, drugs and other disease states: "Patients with alcoholism, migraine, postoperative pinealoma, panhypo-pituitarism, hereditary dystonia and schizophrenics on propranolol exhibited a decreased amplitude of their diurnal rhythm of melatonin." (Wetterberg L J Neural Transm Suppl. 1978;(13):289-310.)
--Fibromyalgia 31% less compared with healthy controls
--Alcohol consumption lowers Melatonin secretion 20% (HHHhhhmmmm...Patrone's+PEET*s apparently is a bad combo for my melatonin??? darn; don't worry -- light intake's fine)
--Obstructive sleep apnea







We are certainly learning a lot about the how all hormones are inter-related in the body. Like life, one disjointed connection can lead to impaired connections downstream. Are there ways to repair and strengthen the misconnected parts? I'm here at TYP...so I certainly believe in the plasticity of our bodies (and I aint referring to the wonders of silicon *wink*).

Thoughtful-mindfulness...meditation, prayer, yoga, tai-chi, massage, day-spa visits all achieve a level of control that is exerted on our 'third eye', the tiny pineal gland (see above; courtesy of here). I read a TIME magazine article ~2-3 yrs about how Buddhist monks were able to activate and light up parts of the brain on PET scans that normally are not associated with neural activity. They meditated (and according to the Dalai Lama teachings that I've read, this involves heightened awareness and enlightened empathy). Is this related to the Pineal Gland? Are there mechanisms that exist for synergizing our Pineal (found in the 3rd ventricle of the brain) with the rest of the brain, body and our deep unconsciousness? (like syncing an iPod to the computer?)

I dunno...but certainly other forms of meditation have been shown in small trials to result in significantly higher melatonin secretion from the Pineal Gland. Like a power nap an adequate night's slumber, how can plain old brain-power power up and protect our Pineal Gland? Apparently in very very very potent ways...! Maybe this justifies my addiction to day spas and yoga?

Tranquility is so super addictive.

Are we hard-wired for tranquility? Yes, I believe so once we are plugged into it.



Plaque-Busting Benefits of Yoga and Meditation
--"Experienced meditators practising either TM-Sidhi or another internationally well known form of yoga showed significantly higher plasma melatonin levels in the period immediately following meditation compared with the same period at the same time on a control night." (Sali A. Acute increases in night-time plasma melatonin levels following a period of meditation. Biol Psychol. 2000 May;53(1):69-78.)
--"Yogic practices for 3 months resulted in an improvement in cardiorespiratory performance (orthostatic tolerance, heart rate, BP, respiratory rate, dynamic lung function (such as forced vital capacity, forced expiratory volume in 1 second, forced expiratory volume percentage, peak expiratory flow rate, and maximum voluntary ventilation) and psychologic profile. The plasma melatonin also showed an increase after three months of yogic practices. The systolic BP, diastolic BP, mean arterial pressure, and orthostatic tolerance did not show any significant correlation with plasma melatonin. However, the maximum night time melatonin levels in yoga group showed a significant correlation (r = 0.71, p less than 0.05) with well-being score. Effects of Hatha yoga and Omkar meditation on cardiorespiratory performance, psychologic profile, and melatonin secretion. Sawhney RC J Altern Complement Med. 2004 Apr;10(2):261-8.)




Coronary/Vasculature Relationship and Role of Melatonin
Two publications from Northwestern med school recently reviewed the melatonin and the receptors that it binds and modulates: MT1, MT2, MT3. In one, the authors described the broad spectrum effects of Melatonin on a variety of organ systems (Masana MI Front Biosci. 2003 Sep 1;8:d1093-108. Molecular pharmacology, regulation and function of mammalian melatonin receptors). Like adrenaline (ie, NE/EPI) that binds beta- or alpha-receptors in various locations in our bodies, the end result can be inhibiting or stimulating activity; the physiological function depends on the location of the receptors as well. Likewise with Melatonin and the MT series, location and type of receptors determines function. Melatonin receptors affect every organ system: CNS (brain), hypothalamic-pituitary-pineal-thyroid-gonadal axis, cardiovascular, and immunity. The second article below describes inhibitory and activating effects of MT receptors.

Functional MT1 and MT2 melatonin receptors in mammals.
Dubocovich ML, Markowska M. Endocrine. 2005 Jul;27(2):101-10.

Melatonin, dubbed the hormone of darkness, is known to regulate a wide variety of physiological processes in mammals. This review describes well-defined functional responses mediated through activation of high-affinity MT1 and MT2 G protein-coupled receptors viewed as potential targets for drug discovery.

MT1 melatonin receptors modulate NEURONAL FIRING, ARTERIAL VASOCONSTRICTION, cell proliferation in cancer cells, and REPRODUCTIVE AND METABOLIC FUNCTIONS.

Activation of MT2 melatonin receptors phase shift circadian rhythms of neuronal firing in the suprachiasmatic nucleus, inhibit dopamine release in retina, INDUCE VASODILATION and inhibition of leukocyte rolling in arterial beds, and ENHANCE IMMUNE RESPONSES.

The melatonin-mediated responses elicited by activation of MT1 and MT2 native melatonin receptors are dependent on circadian time, duration and mode of exposure to endogenous or exogenous melatonin, and functional receptor sensitivity. Together, these studies underscore the importance of carefully linking each melatonin receptor type to specific functional responses in target tissues to facilitate the design and development of novel therapeutic agent. (OF COURSE! LET'S MAKE A PROFITABLE DRUG! ESP WHEN A CHEAP NATURAL ORIGINAL ALREADY EXISTS AND IS WIDELY AVAILABLE)
PMID: 16217123

And btw...STOP WHEAT
In polyglandular autoimmune thyroiditis (hypothyroidism), melatonin levels were naturally found to be low particularly when more fatigue was observed by the study participants. The more fatigue, additionally, the more auto-antibodies were found associated with more organs. The adrenals were attacked in addition to the ovaries, thyroid and/or TPO (thyroid peroxidase). It is not clear precisely the relationship between thyroid function, melatonin and auto-antibodies here... In trials looking at simple hypothyroidism, often melatonin levels are fine or mildly shifted. In the case where multiple glands/organs are affected, the melatonin effects appear more significant. I never realized we could make auto-antibodies to our adrenals. But the medical literature is chock full of stories of auto-antibodies produced against nearly ANYTHING in our bodies -- including our p450 enzymes and even...(!!) mitochondria (our little nuclear ATP powerhouses).

??Can we possibly produce auto-antibodies to our pineal? Or calcify it to rock or pebble? Why not? I believe we could...

Wheat as you aware is not only a common food allergen, but it increases gene expression (62 in this trial detected) of a variety of stress hormones, cytokine-chemokine–mediated immunity, and the interleukin pathway, and MMPs (metalloproteinases) (prior post on the FUNGENUT study). Does wheat trigger the increased production of auto-antibodies? Absolutely. Hypothyroidism is a common autoimmune manifestation of silent celiac disease, in other words wheat intolerance. Other organs or tissues frequently 'burnt to a toast' include: Fingers/Rheumatoid; Wrists/CTS; Knees/osteoarthritis; Gallbladder/biliary dz; Insulin receptors/Type 2 Diabetes; Pancreas/Type 1 Diabetes; Ovaries/infertility; Spit glands/Sjogrens; Myelin/MS; et cetera. How about Muscles/fibromyalgia? The Brain?? Consideration of complete wheat cessation is necessary I believe to prevent burning out multiple organs (including the coronary vasculature).

[The fatigue syndrome in autoimmune thyroiditis with polyglandular activation of autoimmunity][Article in Czech]
Zamrazil V et al.Vnitr Lek. 1998 Aug;44(8):456-60.

The authors compared in a group of 118 patients with autoimmune thyroiditis and a positive antibody titre against ovaries the grade of fatigue with the presence of organ specific and non-specific autoantibodies in the peripheral blood stream, antibodies against EBV and CMV, immunoglobulin concentrations, biochemical parameters of the lipid metabolism, glucose tolerance, ion balance and melatonin and serotonin levels. Patients with autoimmune thyroiditis were differentiated according to the degree of fatigue into three groups: 38 with fatigue typical for CFS (chronic fatigue syndrome), 30 with occasional fatigue and 50 without the feeling of fatigue. Fatigue of the CSF type was characterized by a significantly higher incidence of autoantibodies against the adrenals and a higher cholesterol level. Increased fatigue of the patients was associated with a lower melatonin level, a higher serotonin level and a lower M/S ratio as compared with patients without fatigue. In other indicators no differences were found. Fatigue in CFS could be associated, similarly as in autoimmune endocrinopathies, with impaired immunoendocrine regulation. In autoimmune thyroiditis, regardless of the concomitant presence of fatigue, in addition to antibodies against thyroid peroxidase most frequently antibodies against the ovaries were detected.
PMID: 10358448