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

Hot Pink Kraut in The New Kitchen

Hot Pink 'Kraut!

Made by My Kids

We moved and it's been hectic. This past summer, my kids were so fortunate to attend the most jiving cooking class at the Albany Community Center in Northern California, where their sweet teacher Ilah Jarvis is not only a Baumann College Nutrition graduate but also an integrated practitioner. They learned all the basics for soaking and cooking nuts, (GF) grains and legumes, dairy-free pesto, meats, salads, dressings, sides, and spent ONE WHOLE DAY on the benefits and techniques of fermenting vegetables (kim chee, sauerkraut, pickles).

Their second batch of hot pink kraut is in the crock (gift from our Fujian ayi) and bowl. You fill the moat at the top with water to provide a tight seal that allows anaerobic fermentation.  Formed gas can escape one-way across the seal.  I used the old 'kraut as a starter for our inaugural batch at the new abode in the burbs.  (Yes we are outta the grind and grime of the Shanghai Pudong city...) This recipe below is my daughters' favorite because it tastes like kim chee but sans spiciness.  I had no idea how easy, inexpensive and gratifying it is to eat your own 'kraut... In the States, I fell in love with Sonoma Brinery's RAW SAUERKRAUT this summer.  Was so pleased I could find it in fresh supply everywhere (WH, Andronico's, etc).  Though we love it but kraut is a bit of work -- need a minimum 3 hours to prepare 1-2 weeks worth (one person; for 2 kids = 2 hours + undisclosed hours clean up (MOM)).  However, it's so guuuuud...we eat it almost as fast as it's made...

Tickled Pink Ginger Kraut (adapted from HERE)

Ingredients
1 Head Green Cabbage
2 Heads Purple Cabbage
6 Carrots
4-5 tbsp Sea Salt
2-4 tbsp Fresh Garlic
1 Lemon Squeezed

Combine and squeeze squeeze squeeze.  Minimizes the juicing out and 'organic explosions' later, as my kids told me.  If you add a starter, days on the counter is shortened to only 3 days, otherwise 5-7 days at room temp is needed to get a good ferment going.  Sander Katz's book Wild Fermentation is awesome for more ideas.










New science media on the microbiome and evolution...



(1) Convergent Evolution of Hyperswarming Leads to Impaired Biofilm Formation in Pathogenic Bacteria (hat tip: NB)

Cell Reports, Volume 4, Issue 4, 697-708, 15 August 2013

AuthorsDave van Ditmarsch, Kerry E. Boyle, Hassan Sakhtah, Jennifer E. Oyler, Carey D. Nadell, Éric Déziel, Lars E.P. Dietrich, Joao B. Xavier
HighlightsExperimental evolution of swarming in P. aeruginosa generates hyperswarmers
Parallel evolution in the flagellar regulator FleN is causal for hyperswarming
Point mutations in FleN produce multiflagellated hyperswimming bacteria
There is an evolutionary trade-off between motility and biofilm formation
SummaryMost bacteria in nature live in surface-associated communities rather than planktonic populations. Nonetheless, how surface-associated environments shape bacterial evolutionary adaptation remains poorly understood. Here, we show that subjecting Pseudomonas aeruginosa to repeated rounds of swarming, a collective form of surface migration, drives remarkable parallel evolution toward a hyperswarmer phenotype. In all independently evolved hyperswarmers, the reproducible hyperswarming phenotype is caused by parallel point mutations in a flagellar synthesis regulator, FleN, which locks the naturally monoflagellated bacteria in a multiflagellated state and confers a growth rate-independent advantage in swarming. Although hyperswarmers outcompete the ancestral strain in swarming competitions, they are strongly outcompeted in biofilm formation, which is an essential trait for P. aeruginosa in environmental and clinical settings. The finding that evolution in swarming colonies reliably produces evolution of poor biofilm formers supports the existence of an evolutionary trade-off between motility and biofilm formation.

(2) How hormones and microbes drive the gender bias in autoimmune diseases (hat tip: Angela)

Immunity, Yurkovetsky et al.: "Gender bias in autoimmunity is influenced by microbiota." Free PDF.

Sex hormones are known to play an important role in the gender bias of autoimmune diseases. But studies have shown that environmental influences and other non-hormonal factors also make a difference. For instance, animals that lack gut microbes because they were raised in a germ-free environment do not show a pronounced gender bias in type 1 diabetes, which is generally considered to be an autoimmune disorder. Until now, it has not been clear how hormones and microbes work together to influence the gender bias in type 1 diabetes and other autoimmune diseases.
In the new study, Chervonsky and his team found that microbial communities in male and female mice became different once the mice reached puberty, whereas microbes in females and castrated males were more similar to each other. These results suggest that sex hormones contribute to gender-specific changes in microbial communities. When the researchers raised mice in a germ-free environment and then exposed them to different types of bacteria, they discovered that only certain microbes specifically protected males against type 1 diabetes.
Taken together, the findings suggest that hormones and microbes cooperate with each other to protect males against autoimmune diseases. "Our study has helped to establish the general principles of how hormones and microbes interact with the immune system, which is the first significant step to get to the stage of developing new therapies."

I find this umbrella publication of multiple mouse experiments really fascinating and neat as it found robust and vigorous testosterone levels to be protective for male mice against the Type 1 Diabete (T1D)  mouse model (usually it is high estrogens -- E1 E2 4OHE1 16OHE1 etc).  I wish these researchers measured the estrogens in these mice because the picture seems incomplete...

Segmented filamentous bacteria (SFB) were the population found to be not only most protective but also associated with the highest testosterone levels in male mice.  It appeared to elevate mouse androgen concentrations to a threshold necessary for autoimmunity protection.  Can poor gut flora knock out your T?  Also interestingly, the commercial VSL #3 frequently used therapeutically for IBS, Crohn's and other GI disorders was found (again, remember, in mice) to be associated with lower T.  That was an odd finding as VSL #3 is high in Lactobacillus and other strains typically associated with balanced flora.

SFB and Autoimmunity

Photo Credit: Ivanov, Littman 2010

We know already that gut dysbiosis and anything excessively taxing raises cortisol which can sap and suck the steroids out testosterone (for males) and progesterones (for females), if chronic and enduring.  When this dysregulation occurs, inflammatory estrogens are favored over metabolism of anti-inflammatory estrogen moieties. Estrogen has a role as a stress signal across both plant and animal kingdoms. Some of our best antioxidants (EGCG, curcumin, genistein, resveratrol) are weak phytoestrogens synthesized by plants in response to stressors.  In every chronic disease -- prostate cancer, breast cancer, hypertension, heart disease (TACT), osteoporosis, PCOS, infertility, autoimmunity -- endogenous inflammatory hydroxyestrogens and/or xenoestrogens/metallo-estrogens are either elevated or outweigh the beneficial the estrogens (2-OHE1, etc).

Intimate Crosstalk Between SFB
With Intestinal Cells

(photo credit: Nature)

Heretofore virtually undiscovered in humans (only insects and many mammals), earlier this year 2013, Yin et al in Hangzhou, China characterized one of the earliest human commensal SFB. Via 16S rRNA-specific PCR detection, the intestinal contents of 251 humans, 92 mice and 72 chickens were analyzed. The researchers state "The results showed SFB colonization to be age-dependent in humans, with the majority of individuals colonized within the first 2 years of life, but this colonization disappeared by the age of 3 years... In summary, our results showed that SFB display host specificity, and SFB colonization, which occurs early in human life, declines in an age-dependent manner." Formerly known as 'Candidatus Arthromitis' , like 80-90% or more of our intestinal microbiota, they are unculturable anaerobic bacteria.  SFB hail from the Firmicutes phylum (Order: Clostridia). Like many of the good gut flora they appear to play instructive roles in stimulating proper TH17 and Treg responses in for immune fitness. We need some Firmicutes -- not a ton as it is overdistributed in nearly every obesity microbiota analysis compared with Bacteroides (or it can be too low and eclipsed by Bacteroides) -- but an adequate and sufficient amount it seems and the right kind appear good. Might there be a spectrum of good v. bad Firmicutes like all things? Can 'kraut and other fermented veggies help add the good anaerobic micro critters?  I hope so.

One analysis using pyrosequencing techniques to quantify and identify the microbial composition of traditional Korean fermented kochujang which is a ubiquitious condiment made of of red pepper, glutinous rice, salt, soybean and the naturally occurring microanimalia (e.g. dirt organisms). Of the 223 species discovered, 93.1% were Firmicutes, including Bacillus subtilis, a strain known to digest gluten and casein (as also found in traditional sourdough and other fermented foods). YUM! Gochujang is the hot pepper paste for bibimbap.  Modern, post-industrial gochujang actually is tainted by high amounts of gluten/wheat as a filler, flavor, preservative and 'spice' unfortunately.  FYI, for the real stuff, find a Korean market and look in the refridgerated area.

Death of the Great Cholesterol Diet Fairy Tale, Familial Hypercholesterolaemia, BRCA1/2 Myths, Insulin 101, Cancer and 50 Shades of F_cked (Sorry, Y E S Again)

Sorry for the delay.... Old scathing editorial in QJM (hat tip: Peter D'Adamo), by D.D. Adams 'The great cholesterol myth; unfortunate consequences of Brown and Goldstein’s mistake.'



The Mistaken Implication of FHC and Elevated Blood Cholesterol

Abstract  Following their Nobel Prize-winning discovery of the defective gene causing familial hypercholesterolaemia, Brown and Goldstein misunderstood the mechanism involved in the pathogenesis of the associated arterial disease. They ascribed this to an effect of the high levels of cholesterol circulating in the blood. In reality, the accelerated arterial damage is likely to be a consequence of more brittle arterial cell walls, as biochemists know cholesterol to be a component of them which modulates their fluidity, conferring flexibility and hence resistance to damage from the ordinary hydrodynamic blood forces. In the absence of efficient receptors for LDL cholesterol, cells will be unable to use this component adequately for the manufacture of normally resilient arterial cell walls, resulting in accelerated arteriosclerosis. Eating cholesterol is harmless, shown by its failure to produce vascular accidents in laboratory animals, but its avoidance causes human malnutrition from lack of fat-soluble vitamins, especially vitamin D.

Unfortunate consequences of Brown and Goldstein’s mistake

Brown and Goldstein’s burst of fascinating information dazzled the medical profession, most of whom consequently accepted the false cholesterol hypothesis. This has led to unfortunate consequences that include:

• Waste of money on misdirected research.
• Waste of money on blood cholesterol tests.
• Waste of money on statins.
• Malnutrition from lack of fat-soluble vitamins (A,D,K,E) present in butter, full-cream milk and animal fat but lacking in margarine and skim milk (green-top bottles in New Zealand).
• Fear of eating eggs, contributing to unhealthy, starchy diets.
• Ricketts in middle-aged men from lack of vitamin D due to use of margarine and skim-milk.
• Distortion of the Dairy Industry, causing unnecessary marketing of skim milk.
• Distortion of the Meat Industry with unnecessary production of lean meat.

The author concludes 'The fact that of the thousands of people involved in achieving this spurious result did not include a single elementary mathematician with intellectual independence is in accord with the whole sorry story of the great cholesterol myth, starting with the false statistics used in analysing the Framingham data.10 The meta-analysis of Ray et al.,13 showing no prolongation of life by use of statins in randomized controlled trials involving 65 229 participants, is the final nail in the coffin of the great cholesterol myth.'



Insulin 101, Diabesity and Cancer Malignancies....

The lifetime risk of developing any invasive cancer is over 1:3 (males nearly 1:2) currently and by 2020, the WHO estimates, the stats will be 1:2 for both males and females.  The XX chromosomes no longer will protect us gals.

Why?

Does it have anything to do with 'Great Cholesterol Diet Myth' that the above authors have dispelled on unfounded, false scientific interpretations?  The refined whole-wheat-unhealthy-heart debacle may be nearing its end after this editorial, perhaps.

Is our diabesity and cancer epidemics related to the growth over the last few decades of 'low fat,' government-sanctioned, high refined carbs, grain-based propaganda and GMO (Bt-gut busting zonulin-opening lectins), pesticide laced grains and grain-fed commercial meat, poultry, dairy and eggs?  And the environmental havoc that plays out...?  Our original gut flora are nearly extinct much like most of the rainforest species.  Compound this with other endocrine- and gut-disrupting toxins like mercury and arsenic that  rain out from coal burners which still supply greater than 50% of USA energy.  BTW China is now #1 globally for coal utilization, eeking out over the USA in recent years. Go China for exceeding USA's giant industrial pollution footprints.

http://www.avonbreastcare.org/files/SusanLuckWebinar.pdf

BRCA1/2 and Chopping Off B**bies

Breast cancer is complex, yet it is quite simple. Is it necessary to contemplate IMHO surgical removal and reconstruction of any beautiful body part that may fall to cancer? Where does one logically start? Where does one end because everything that undergoes DNA replication and editing may fall to cancer and mutations...?  Ms. Angelina Jolie, I lurrv u, please stop. Your message is IMHO short-sighted and not sustainable.




Pardon, Let's Look at A Couple of BRCA1/2 Facts: 

BRCA1/2 is a defect in DNA repair and fails to fix 8OHdG (oxidative DNA damage product, 8-hydroxy-2'deoxyguanosine)

BRCA1/2 raises risk in men of breast, prostate, pancreatic, gastric and hematologic cancers

BRCA1/2 raises risk in women of breast (73%), ovarian (41%), colon (2-fold), pancreas (3-fold), stomach (4-fold) and fallopian tube (120-fold) cancers

BRCA1/2 like all mutation genes is under epigenetically controlled regulation -- for example, silencing of the gene occurs with polyaromatic hydrocarbons (pollution), insulin, and hypomethylation (lack of methyl donors -- either depletion or dietary deficiency -- or COMT, MTHFR, etc variants). Best food sourced methyl donors are methylB12, choline and methylfolates (free range egg yolks, liver, meat, seafood -- sorry no plant sources you crazy vegans).  Insulin 101: Insulin is a growth hormone and one function is to induce stimulation of female ovaries to increase testosterone secretion.  Unfortunately, in both men and women, normal levels and excess testosterone may be converted into estrogens under insulin induction by P450-aromatase (aka, CYP19), in many tissues including fat tissues, breast cells, endothelial cells and prostate cells.... Certain gene variants accumulate significantly more estrogens than non-carriers (COMT, CYP19).

• Compared with noncarriers, women carrying at least one CYP19 8r allele had 20% higher estrone (P = 0.003), 18% higher estradiol (P = 0.02), and 21% higher free estradiol concentrations (P = 0.01). Women with the COMT Met/Met genotype had 28% higher 2-hydroxyestrone (P = 0.08) and 31% higher 16α-hydroxyestrone concentrations (P = 0.02), compared with Val/Val women. Cancer Epidemiol Biomarkers PrevJanuary 1, 2004 13; 94.

BRCA1/2 silencing may be epigenetically avoided by diet, resveratrol and other antioxidants

BRCA1/2 needs a genetic 'cofactor' like MTHFR, COMT, CYP19 (aromatase which converts testosterone to estrogens), CYP1B1 (pathway increases 16OHE1, estrogen carcinogen adduct) and CYP1A1 to be carcinogenic according to emerging evidence. These genetic polymorphisms are all related to raised toxic estrogen metabolites and creation of estrogen dominant states.

Functional Medicine and Tracking/Lowering 8OHdG

GDX/Metametrix Labs and other functional medicine lab testing centers offer a wonderful test that measures and helps practitioners to track oxidative DNA damage, the 8OHdG biomarker.  This goes up and down with oxidative damage. Many things have been shown to lower and raise 8OHdG.  Diet and supplements (melatonin, vitamin C, berry extracts, resveratrol, etc) have been shown to lower 8OHdG.  Please check out more HERE and HERE (p. 361 of 'Lab evals for integrative and functional medicine' 2nd ed, 2008).

In a hepatitis C trial in participants at risk for hepatic carcinoma and iron overload, a low-iron diet and phlebotomy lowered 8OHdG to near normal 8OHdG rates after 6 yrs. Additional observed benefits were improvements in liver function: lower ALT and liver function tests, improved scarring and hepatitis, no progression to carcinoma. Viral Hep C titers remained the same but cancer was avoided despite originally sky-high 8OHdG six years prior at trial onset.



Prior animal pharm:

Pesticides May Be Behind USA Diabesity, Disrupting Insulin and Tissue Insulin Resistance
50 Shades of F_cked Up (Cancer medical management in the USA)



Other Citations:

http://www.ultrawellnesscenter.com/files/2010/05/Functional-Diagnostics-Redefining-Disease.pdf
http://www.ultrawellnesscenter.com/files/2010/05/Cholesterol-AT.pdf
http://www.cancer.org/cancer/cancerbasics/lifetime-probability-of-developing-or-dying-from-cancer
http://whattofeedyourkids.blogspot.jp/2009/10/xenoestrogens-and-breast-cancer-why-we.html
http://www.scientificamerican.com/article.cfm?id=earth-talk-the-coal-truth

http://www.lef.org/magazine/mag2012/nov2012_Epigenetics_Breast_Cancer_01.htm
Aromatase up-regulation, insulin and raised intracellular oestrogens in men, induce adiposity, metabolic syndrome and prostate disease, via aberrant ER-α and GPER signalling.
MTHFR Polymorphisms, Dietary Folate Intake, and Breast Cancer Risk Results from the Shanghai Breast Cancer Study [hat tip: Todd Lepine MD]
Breast. 2008 Oct;17(5):441-50. Counseling for male BRCA mutation carriers: a review.
Methionine-Dependence Phenotype in the de novo Pathway in BRCA1 and BRCA2 Mutation Carriers with and without Breast Cancer. [need for methyl donors]
Epigenetic diet: impact on the epigenome and cancer.
Dietary phytochemicals, HDAC inhibition, and DNA damage/repair defects in cancer cells.
Epigenetic impact of dietary polyphenols in cancer chemoprevention: Lifelong remodeling of our epigenomes.

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.

Shanghai Talk: Balancing Hormones To Improve Mood, Energy, Body Fat and Breast Cancer Prevention

Miracle
OceanLab, Above and Beyond

I have a talk in Shanghai coming up FYI...You are invited!


Topic: Balancing Hormones To Improve Mood, Energy, Body Fat and Breast Cancer Prevention

Functional/integrative medicine resources:

http://drhyman.com/blog/2010/04/28/ultrawellness-lesson-5-detoxification/ http://drhyman.com/blog/2010/05/21/breast-cancer-how-to-reduce-your-risk-now-2/

http://www.imjournal.com/resources/web_pdfs/popular/1008_evans.pdf

Pesticides in Shanghai and Globally

Titanium (Cover of Sia, David Guetta)
Collin McLoughlin

Pesticides -- Shanghai Problem

Pesticides, herbicides and fungicides are big problems here in Shanghai. Apparently we live in the city with the highest reported field application of pesticides (kilograms per hectare) out of the whole country. According to the report by Zhang et al 'Global pesticide consumption and pollution: with China as a focus' Shanghai applies 12.72 kilograms per hectare of pesticides, which was the heaviest utilization of 32 cities and provinces studied. The lowest utilization rates were in the least industrialized provinces, Inner Mongolia and Tibet (0.15, 0.01 kg/ha respectively).

Prior animal pharm: Pesticides May Cause U.S.A. Insulin Resistance and Obesity Trends





Pesticides are (Obviously) Toxic and Kill

Pesticides, herbicides and fungicides may not be lethal to large mammalian hosts like humans but the mechanisms in which they wreak chemical havoc to pests, weeds/grasses and fungus/molds can affect us either directly or our gut ecosystem which contains 100 trillion mitochondrial-like creatures (bacteria, mycobacteria, protozoa) and fungi. ~~Half of the deaths that occur worldwide secondary to pesticide exposures are here in China. 'According to a report of WHO and UNEP, worldwide there are more than 26 million human pesticide poisonings with about 220,000 deaths per year (Richter, 2002). In the United States, there are 67 thousands human pesticide poisonings per year. In China, there are 0.5 million human pesticide poisonings with 0.1 million deaths per year. (Zhang et al 2011)'

The mechanisms of toxicity of pesticides, herbicides and fungicides usually target a specific neurochemical or metabolic mechanisms that translate toxicity to the cellular, organ and organismal levels:
--sodium channel disturbances (yes our sodium channels are vital; see prior nephropal Evolutionary Brain)
--glyphosate toxicity (see Dr. Tourgeman's nephropal post: Can Glyphosate Herbicide Formulations Damage Humans?)
--mitochondrial toxicity -- electron transport
--mitochondrial toxicity -- fatty acid metabolism
--mitochondrial toxicity -- respiratory complex
--trace heavy metals -- mercury, asenic, cadmium and lead --which severely depress metabolic enzymes (mitochondrial, thyroid, adrenal, neural, gut i.e. DPP IV, pancreatic/digestive, etc)




Pesticides: Global Problem

Although the knowledge and understanding are incomplete, the data and information on how pesticides, herbicides and fungicides are transported, degraded and distributed into the ecosystem are pretty damning. The toxicity effects may not immediately disable and maim but may be chronically sublethal and epigenetic. Since all life on earth is interconnected, the network of disturbances can be subtle. Damaging effects perhaps act in concert either additively or synergistically with other stressors, gut dysbiotic factors and amplified by our trigger-happy immune systems. Zhang et al say that 99% of pesticides, herbicides and fungicides do not even hit the intended target. 99% of pesticide applications are distributed into the environment and ecosystem by spray drift and surface water runoff. The investigators Zhang et al state 'High-residual pesticides like DDT have been detected in the Greenland ice sheet and the bodies of Antarctic penguins which were resulted from atmospheric circulation, ocean currents and biological enrichment of pesticides.' The early players of the damage and adverse effects are the bees, insectal larvae and algae on land and in related water masses. In the next tier of ecological effects, their predators (insects, fish, sealife) are affected either indirectly by reduction of food availibility or direct biochemical, metabolic, immune, endocrine, sexual and reproductive disruptions.

And... Up and up the PREDATOR ECOSYSTEM CHAIN.

[I doubt humans can claim being apex predators, but perhaps apex pests and homo purgare]



Fish: One of the Most Pesticide-Ridden and Toxic Foods

My family and stopped eliminated 80-90% of our fish and seafood consumption (both farmed and wild) when I was first pregnant 12 years ago. I figured what wasn't safe for my baby and I just was not safe, PERIOD. We try to eat ancestrally but seafood just is not part of the equation at this time. Many cultures who subsist on fish and their marine predators (seal, whale) are documented to have elevated levels of persistent organic pollutants (POPs, pesticides, PCBs, solvents, etc) and heavy metals: Great Lake Anishinaabe, Arctic and Greenland Inuit, natives of the Alaskan Aleutian Islands, Amazon Brazilians, Peruvians, and Faroe Islands inhabitants. Where is the source? Pesticides and industrial pollution are bioaccumulated in algae, daphnia, marine life and large predacious fish and marine mammals. Human variance shows that not everyone is severely affected by heavy metals (mercury) and pesticides but certainly some are more sensitive than others or bioaccumulate at extremely higher rates than other individuals. The carriers of apo E4 allele, the ancestral 'efficiency' allele, appear to exhibit higher harboring and decreased detoxification of trace heavy metals (iron, copper, lead, mercury). This may explain the link between increased incidence of central obesity, metabolic syndrome, T2DM, Alzheimer's and dementia and those of ethnic descent where the apo E4 allele is more dominant (Inuit, Amerindians, aborigine subpopulations, northern Chinese, northern European, Africa).



The Jungle: Food Safety in China

Living in China has many 'challenges' (I could list but that would be a brick of novella) but I would have to say food safety TOPS my MANY MANY MANY lists. On one hand Shanghai is one of the most progressive cities of the world I have been fortunate to visit (Paris, Hamburg, NYC, Chicago, SF, Tokyo, Kyoto, Taipei) yet in the context of food safety and standards of quality, I think it is one of the cities with the least quality control and national oversight. For every daily food safety scandal that hit the media, I always wonder how many dozens didn't hit the media under China's scrupulous censorship. We live here in the times that pre-date Upton Sinclair's 'The Jungle' (free PDF HERE, courtesy of Penn State).

Super wonderful people here in Shanghai have been graciously generous in sharing their food suppliers ('The Avocado Lady'), chains of safe food purveyors and organic grassfed meat and egg sources, CSAs (see picture BIOFarm) and safe homemade goodies. Part of the adventure of expat living has been meeting other like-minded freaks in a foreign country.





References

Global pesticide consumption and pollution: with China as a focus. Zhang et al. Proceedings of the International Academy of Ecology and Environmental Sciences, 2011, 1(2):125-144.

Greenpeace 2009 News. Pesticides: Not Your Problem?
http://www.greenpeace.org/eastasia/news/China-pesticides/

Medscape, Maternal Fish Consumption, Mercury Levels, and Risk of Preterm Delivery: Discussion
http://www.medscape.com/viewarticle/553133_4

Is "USDA Organic" a seal of deceit? The pitfalls of USDA certified organics produced in the United States, China and beyond.

Mercury Toxicity and Treatment: A Review of the Literature. Robin A. Bernhoft. J Environ Public Health. 2012; 2012: 460508.

Sources of Mercury Exposure for U.S. Seafood Consumers: Implications for Policy. Noelle E. Selin, Elsie M. Sunderland, Christopher D. Knightes, Robert P. Mason. Environ Health Perspect. 2010 January; 118(1): 137–143.

The influence of nutrition on methyl mercury intoxication.L Chapman, H M Chan. Environ Health Perspect. 2000 March; 108(Suppl 1): 29–56.

Neurobehavioral effects of developmental methylmercury exposure.[low chronic levels cause neurologic effects] S G Gilbert, K S Grant-Webster. Environ Health Perspect. 1995 September; 103(Suppl 6): 135–142.

New Evidence on Variations of Human Body Burden of Methylmercury from Fish Consumption.René Canuel, Sylvie Boucher de Grosbois, Laura Atikessé, Marc Lucotte, Paul Arp, Charles Ritchie, Donna Mergler, Hing Man Chan, Marc Amyot, Robin Anderson. Environ Health Perspect. 2006 February; 114(2): 302–306.

Impacts of traditional food consumption advisories: Compliance, changes in diet and loss of confidence in traditional foods. Claire McAuley, Loren D Knopper. Environ Health. 2011; 10: 55.

The Changing Landscape of Arctic Traditional Food. Tim Lougheed. Environ Health Perspect. 2010 September; 118(9): A386–A393.

Apolipoprotein E (APOE) allele distribution in the world. Is APOE*4 a 'thrifty' allele? Corbo RM, Scacchi R. Ann Hum Genet. 1999 Jul;63(Pt 4):301-10.

Apolipoprotein E and atherosclerosis in Greenland Inuit. Boudreau DA, Scheer WD, Malcom GT, Mulvad G, Pedersen HS, Jul E.Atherosclerosis. 1999 Jul;145(1):207-19.

Synergy between the C2 allele of transferrin and the C282Y allele of the haemochromatosis gene (HFE) as risk factors for developing Alzheimer's disease. [the effects areextremely exacerbated in apoE4 carriers] Robson KJ, Lehmann DJ, Wimhurst VL, Livesey KJ, Combrinck M, Merryweather-Clarke AT, Warden DR, Smith AD.J Med Genet. 2004 Apr;41(4):261-5.

Alzheimer disease: mercury as pathogenetic factor and apolipoprotein E as a moderator. Mutter J, Naumann J, Sadaghiani C, Schneider R, Walach H.Neuro Endocrinol Lett. 2004 Oct;25(5):331-9.

An observational study on the influence of the APOE-epsilon4 allele on the correlation between 'free' copper toxicosis and EEG activity in Alzheimer disease.Zappasodi F, Salustri C, Babiloni C, Cassetta E, Del Percio C, Ercolani M, Rossini PM, Squitti R.Brain Res. 2008 Jun 18;1215:183-9.

Bioaccumulation syndrome: identifying factors that make some stream food webs prone to elevated mercury bioaccumulation. Darren M. Ward, Keith H. Nislow, Carol L. Folt. Ann N Y Acad Sci. 2010 May; 1195: 62–83.

Fish Consumption and Advisory Awareness in the Great Lakes Basin. Pamela Imm, Lynda Knobeloch, Henry A. Anderson, the Great Lakes Sport Fish Consortium. Environ Health Perspect. 2005 October; 113(10): 1325–1329.

Evaluation of Mercury Exposure Reduction through a Fish Consumption Advisory Program for Anishinaabe Tribal Members in Northern Wisconsin, Michigan, and Minnesota. J. A. Foran, A. D. DeWeese, M. J. Hudson, N. E. Kmiecik. J Environ Public Health. 2010; 2010: 802584.

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

Elevated Mercury Concentrations in Humans of Madre de Dios, Peru. Katy Ashe. PLoS One. 2012; 7(3): e33305.

Research into Mercury Exposure and Health Education in Subsistence Fish-Eating Communities of the Amazon Basin: Potential Effects on Public Health Policy.José G. Dórea. Int J Environ Res Public Health. 2010 September; 7(9): 3467–3477.

A preliminary study of mercury exposure and blood pressure in the Brazilian Amazon. Myriam Fillion, Donna Mergler, Carlos José Sousa Passos, Fabrice Larribe, Mélanie Lemire, Jean Rémy Davée Guimarães.Environ Health. 2006; 5: 29.

Hydroxylated PCB metabolites and PCBs in serum from pregnant Faroese women.Britta Fängström, Maria Athanasiadou, Philippe Grandjean, Pál Weihe, Ake BergmanEnviron Health Perspect. 2002 September; 110(9): 895–899.

Levels of Polychlorinated Biphenyls (PCBs) and Three Organochlorine Pesticides in Fish from the Aleutian Islands of Alaska.Sara Hardell, Hanna Tilander, Gretchen Welfinger-Smith, Joanna Burger, David O. Carpenter. PLoS One. 2010; 5(8): e12396.

Re-evaluation of blood mercury, lead and cadmium concentrations in the Inuit population of Nunavik (Québec): a cross-sectional study. Julie Fontaine, Éric Dewailly, Jean-Louis Benedetti, Daria Pereg, Pierre Ayotte, Serge Déry. Environ Health. 2008; 7: 25.

Assessment of dietary exposure to trace metals in Baffin Inuit food.H M Chan, C Kim, K Khoday, O Receveur, H V Kuhnlein. Environ Health Perspect. 1995 Jul-Aug; 103(7-8): 740–746.

Determinants of polychlorinated biphenyls and methylmercury exposure in inuit women of childbearing age.G Muckle, P Ayotte, Dewailly E, S W Jacobson, J L Jacobson. Environ Health Perspect. 2001 September; 109(9): 957–963.

Pesticides May Cause U.S.A. Insulin Resistance and Obesity Trends

Emancipator
'Greenland'

Modern Big Tobacco-Agra/Monsatan Crops

Crops are generally coated with pesticides for the last 30-50 years. Are they toxic? Pesticides are upregulated into the food chain via consumption (corn, soy) by feedlot livestock and poultry. Let's not forget tobacco (cigarettes, snuff, cigars, etc). 'Tobacco is a pesticide-intensive crop. With nearly 27 million pounds of pesticides (including insecticides, herbicides, fungicides, and suckercides) applied to the U.S.-grown crop from 1994 to 1998, it ranks SIXTH in terms of the amount of pesticides applied per acre. The tobacco industry regards pesticides as essential to tobacco production, stating that “the crop could not be produced economically without them”.'

Additionally pesticides are employed in municipalities (public schools, parks, government land) and personal home use (termites, ant control, weeds control, lawns, etc). Although pesticides do not taste, smell or look toxic, they are not benign and without metabolic dysregulation consequences.

New studies in PubMed are cropping (pun intended) up in number pointing directly to insulin resistance, obesogenic, neurologic and inflammatory damage secondary to this broad group of pervasive chemicals known as persistent organic pollutants (POPs). They are difficult to avoid as once in the soil, air or bodies of water, fish, birds and animals, they typically fail to degrade and significantly impact the environment.

The researcher Alavanja states 'Over 1 billion pounds of pesticides are used in the United State (US) each year and approximately 5.6 billion pounds are used worldwide (1). In many developing countries programs to control exposures are limited or non-existent. As a consequence; it has been estimated that as many as 25 million agricultural workers worldwide experience unintentional pesticide poisonings each year (4). In a large prospective study of pesticide users in the United States, the Agricultural Health Study, it was estimated that 16% of the cohort had at least one pesticide poisoning or an unusually high pesticide exposure episode in their lifetime (5).

Although attempts to reduce pesticide use through organic agricultural practices and the use of other technologies to control pests continue, exposure to pesticides occupationally, through home and garden use, through termite control or indirectly through spray drifts and through residues in household dust, and in food and water are common (6). The US Department of Agriculture has estimated that 50 million people in the United States obtain their drinking water from groundwater that is potentially contaminated by pesticides and other agricultural chemicals (7, 8). Children from 3-6 years old received most of their dermal and non-dietary oral doses from playing with toys and while playing on carpets which contributed the largest portion of their exposure (9-12).'

U.S.A. Obesity Trends With Pesticide Use

Guess what?

Pesticide use on crops grown in the South (tobacco) and Mid-West (corn, wheat, soy) trends well with U.S.A. obesity patterns [hat tip: LePine MD]. Above is the trend of obesity that starts mid-1980s then grows exponentially each few years. Maps are from Lim et al and BFRSS data.

Smart people in Korea (Lim et al) report that 'There is an apparent overlap between areas in the USA where the herbicide, atrazine (ATZ), is heavily used and obesity-prevalence maps of people with a BMI over 30. Given that herbicides act on photosystem II of the thylakoid membrane of chloroplasts, which have a functional structure similar to mitochondria, we investigated whether chronic exposure to low concentrations of ATZ might cause obesity or insulin resistance by damaging mitochondrial function.'




Pesticides Kill Pests, Including Our Bug-like Mitochondria

It's therefore not surprising to read about the toxic effects of pesticides on pests whose networked pathways overlap almost precisely with our own cells. Atrazine is a mitochondrial toxin, and our mitochondria are the sole energy generators and powerhouses whether the substrate is glycogen, glucose or fatty acids.




Mitochondrial Dysfunction Causes Fatness and Insulin Resistance (IR)

'A close association between mitochondrial dysfunction and insulin resistance is well established [1]–[3]. In in vitro studies, we found that artificial induction of mitochondrial dysfunction induced insulin resistance [4], [5].' This is discussed by Lim et al. He and his colleagues performed an experiment on rodents. They fed low levels of atrazine to rats then examined lab parameters for insulin resistance (IR). What happened? The higher the dose of atrazine, the higher the obesity and insulin resistance. Atrazine was associated with mitochondrial dysfunction, higher visceral (organ) fat deposition, higher blood glucoses and decreased energy metabolism.

Another group of researchers, Ruzzin et al, tested a similar hypothesis. They fed crude Atlantic salmon oil to rodents and examined IR parameters. They state 'POPs accumulate in the lipid fraction of fish, and fish consumption represents a source of POP exposure to humans (Dougherty et al. 2000; Hites et al. 2004; Schafer and Kegley 2002). Therefore, certain European countries have dietary recommendations to limit the consumption of fatty fish per week (Scientific Advisory Committee on Nutrition 2004).' They discovered similar insulin resistant results when they exposed fat cells in vitro to a POP mixture that mimicked the relative abundance of contaminants found in crude salmon oil. Insulin signalling was broken and impaired.





References

BRFSS, Behavioral Risk Factor Surveillance System www.cdc.gov/brfss

http://www.youtube.com/watch?v=iCNW-NgYZ2s [Obesity trend map and cdc slides]

http://www.cdc.gov/nccdphp/dnpa/obesity/trend/maps/obesity_trends_2006.pdf [BRFSS raw data by state and year]

Pesticides Use and Exposure Extensive Worldwide. Michael C.R. AlavanjaRev Environ Health. 2009 Oct–Dec; 24(4): 303–309.

The Tobacco Industry and Pesticide Regulations: Case Studies from Tobacco Industry Archives. Patricia A. McDaniel, Gina Solomon, Ruth E. Malone. Environ Health Perspect. 2005 December; 113(12): 1659–1665.

Chronic Exposure to the Herbicide, Atrazine, Causes Mitochondrial Dysfunction and Insulin Resistance. Soo Lim, Sun Young Ahn, In Chan Song, Myung Hee Chung, Hak Chul Jang, Kyong Soo Park, Ki-Up Lee, Youngmi Kim Pak, Hong Kyu LeePLoS ONE. 2009; 4(4): e5186.

Persistent Organic Pollutant Exposure Leads to Insulin Resistance Syndrome. Jérôme Ruzzin, Rasmus Petersen, Emmanuelle Meugnier, Lise Madsen, Erik-Jan Lock, Haldis Lillefosse, Tao Ma, Sandra Pesenti, Si Brask Sonne, Troels Torben Marstrand, Marian Kjellevold Malde, Zhen-Yu Du, Carine Chavey, Lluis Fajas, Anne-Katrine Lundebye, Christian Lehn Brand, Hubert Vidal, Karsten Kristiansen, Livar FrøylandEnviron Health Perspect. 2010 April; 118(4): 465–471.

Effect of Endocrine Disruptor Pesticides: A ReviewWissem Mnif, Aziza Ibn Hadj Hassine, Aicha Bouaziz, Aghleb Bartegi, Olivier Thomas, Benoit RoigInt J Environ Res Public Health. 2011 June; 8(6): 2265–2303.