Mind/Body HealthRRCC Holistic Health

Spring 2011

Modern Food OverviewIndustrial agriculture

GMOsPesticides/chemicalsOther environmental effectsSweatshops and hierarchy/slavery

Factory farming and animal treatmentEnvironmental effects

Food addictionInstitutional reality

CorporationsGovernments

Domestication and the energy of foodWaste- 25%

Carbohydrates- 4 cals/gram Complex- starches Simple- sugars

Fats- 9 cals/gram 3 fatty acid chains held together by glycerol (blue in the pic) Saturated (with hydrogens)- solid at room temp

The top two chains in the illustration to the right Mononsaturated- one double bond in FA chain- liquid

The bottom chain of the three in the pic Polyunsaturated- two or more double bonds- liquid Man-made forms- the best ones to avoid!

Partially hydrogenated oils- harm the cell membrane Trans-fatty acids

Also harm cell membrane Damage DNA Promote cancer (CA), inflammation, heart disease (CVD), diabetes (DM) Raise cholesterol

Omega 3 and omega 6 are essential (not made in the body) Proteins- 4 cals/gram

Chains of amino acids Vitamins

Fat-soluble (D, E, A, K) Water-soluble (B-complex and C)

Minerals Water

BasicNutrients

Conventional “Wisdom”How does nutrition affect health? Here’s the mainstream

version:The Fat-Cholesterol Hypothesis (aka Diet-Heart Hypothesis)

Fat and cholesterol are the dietary causes of heart disease (CVD) Later, saturated fat and LDL cholesterol are singled out And, dietary fat raises blood cholesterol, leading again to CVD Lowering these reduces CVD and prolongs life- “heart-healthy foods”

And obesity Surgeon General: “Overweight and obesity result from excess calorie

consumption and/or inadequate physical activity.” And fat has the most calories per gram, so it’s the most fattening Fat makes you fat, and it turns the blood to milky sludge, which

creates atherosclerotic plaquesThis is all common sense. Everybody knows this.This does not withstand scientific scrutiny and serves largely

to advance institutional power and control at the expense of personal, collective, and ecological health.

Which is it really? Check out the evidence and decide for yourself!

A Sea Change William Banting- 1863- Letter on Corpulence

lost 35 lbs. in 9 mos., 50 in the next few months by avoiding sugar and minimizing starch

Medical community skeptical Lancet- “old news,” then “dangerous”: “We advise Mr. Banting, and

everyone of his kind, not to meddle with the medical literature again, but be content to mind his own business.” Then a “fair trial.”

We’re still waiting for this “fair trial” today! “The great progress in dietary control of obesity was the recognition

that meat… was not fat producing; but that it was the innocent foodstuffs, such as bread and sweets, which lead to obesity.” -Hilde Bruch, 1957

For over a century, this was the conventional wisdom! Fats and meat were known as protective foods

Sea change by 1970’s- now carbs “help you lose weight.” Medicine still reactionary- AMA- low carb diets are dangerous-

“bizarre concepts of nutrition and dieting [that] should not be promoted to the public as if they were established scientific principles.” -1973

Even as major conferences were demonstrating their effect at losing weight without hunger!

Now low-fat diets are the Way to prevent heart disease and reduce weight USDA food pyramid- fats and oils “sparingly,” 6-11 servings of grains

The Official Story The nation turned away from grains and cereals and toward fat and

red meat and paid the price The “great epidemic” of heart disease

CVD was rare a century ago, and now it’s the #1 killer in the US Coincided with the “changing American diet”

An increase in meat and fat consumption paralleling the rise in CVD But the surge in heart disease, obesity, and diabetes came along

with the message that fat is bad and carbs are good In the US, average fat intake has dropped from 45% of total

calories to 35% in the last 30 years, and cholesterol has fallen- people are following the message

Without improvements in health- quite the opposite! 2,500 deaths each day from CVD- still the #1 killer Obesity 12-14% of population from 1960’s thru 1980, but in 2004,

1 in 3 Americans obese, another 1 in 3 overweight Diabetes has more than doubled since 1980

From WWII, during the supposed “epidemic,” through the 1960’s, the American diet increased in total fat But mainly vegetable fats, considered “heart-healthy” And increase in vegetables and citrus fruits Decrease in animal fats

Cholesterol Found in all body tissues Essential component of cell membranes Involved in many physiologic processes

Metabolism of human sex hormones Also abundant in atherosclerotic plaques So… it must cause the plaques, right?

Science unable to establish that atherosclerotic patients had more blood cholesterol

Also unable to establish that people with high cholesterol had arteries any more clogged

And, dietary cholesterol has very little effect on blood cholesterol Weight gain and stress raise, exercise and weight loss lower, also fx from sex hormones,

diuretics, alcohol But- doctors could measure the levels as of 1934

And use it to make dietary recommendations Blood sugar and blood insulin couldn’t be measured yet So rather than let patients go to the “medical heretics,” like chiropractors and

homeopaths, and rather than admit they didn’t know the answers, docs support the fat-chol hypothesis to maintain and advance their own power

Ditto the nascent American Heart Association, a public health institution seeking, as institutions do, to maintain and advance its own power Along with the NIH, NHLBI, American Diabetes Assn, and American Obesity Assn, among

others

How Did We Get Here? Ancel Keys- physiologist at U Minnesota- starting 1940’s

Naples (and Madrid)- rich more HD than poor, and rich ate more fat Therefore, dietary fat raises blood cholesterol leads to HD

Study of six countries- the more dietary fat, the more HD mortality- but data available for 22 countries, and the effect vanishes when all are included

Selection (or confirmation) bias- choosing evidence that supports conclusion

Everything else “misinterpreted, irrelevant, or bad data”- like studies of Navajos, Irish immigrants, African nomads, monks, etc, showing no relation btw dietary fat and HD Masai nomadic herders live on milk, blood, and meat, and have blood cholesterol

levels among the lowest ever measured Extensive atherosclerosis, but no HD Cholesterol up when they then ate Western diet First “feedback mechanism to suppress endogenous chol synthesis” Then “The peculiarities of those primitive nomads have no relevance to diet-

cholesterol-CHD relationships in other populations” (“It doesn’t fit our premeditated conclusion, so let’s ignore it.” Note the racism also.)

Debate Skeptics- “show us the science” Proponents- obligation to help patients- need to act- urgency

Press fed the fire also- positive feedback loop Manufacturing stress and fear to manufacture consent

Tale of the Tape- The Evidence1950- Framingham Heart Study- 5100 residents

given physicals, the examined every two years to see who got HDRisk factors- HTN, abnormal EKG, obesity, smoking,

family history- these have proven accurate over timeCholesterol- blood levels over 260 assoc with 5x

greater HD risk than chol under 200- compelling evidence

But- the men who died of HD more likely to have low chol, and little assn for women at all

And (despite NIH preventing publication) men with very high (>300) and very low (<170) chol have same amount and types of dietary fat No correlation btw dietary fat and either blood chol or HD-

true in virtually every study comparing these within a single population

Tale of the Tape 1957- Western Electric Study 5400 male employees- looking at HD among those who ate the most

and the least fat 88 cases of HD- 14 in high-fat group, 16 in low-fat Dietary fat not assoc with death from CHD

So- “If viewed in isolation, the conclusions that can be drawn from a single epidemiologic study are limited. Within the context of the total literature, however, the present observations support the conclusion that the [fat] composition of the diet affects the level of serum cholesterol and the long-term risk of death [from CHD] in middle-aged American men.” (“Our study doesn’t show the effect we need in order to maintain future funding, so we’ll just say that it’s in other studies, so it must still be true.” Yes, these are scientists!) This analysis then cited in AHA and NHLBI (Nat’l Heart, Lung, and

Blood Institute) report The Cholesterol Facts as one of seven “epidemiologic studies showing the link btw diet and CHD [that] have produced particularly impressive results,” … “showing a correlation btw saturated fatty acids and CHD.” (Yes, they said “particularly impressive results,” rewriting history to say that they demonstrated exactly what they failed to show!)

1956- Seven Countries Study- Ancel Keys again And once again picking the countries in advance that he knew would

support the hypothesis

Tale of the Tape Anti-Coronary Club Trial- late 1950’s- comparing saturated with

polyunsaturated- 1100 patients Members on the “prudent diet” had 1/3 the HD of controls But 26 members died, 8 from HD, and only 6 controls, none from HD

UCLA VA 1969- replacing animal fat with vegetable oil- cholesterol down 13%, 66 HD deaths, compared with 96 controls

But 31 CA deaths in experimental group, 17 controls Risk of death equal in two groups

Helsinki study- 1965-71- 2 mental hospitals- cholesterol-lowering diet HD deaths down by half, men (not women) lived a little longer

Minnesota Coronary Survey- 1968- 9000 mental patients Half got American diet, half cholesterol-lowering

Low in cholesterol and saturated fat, high in polyunsaturated Cholesterol down 15%, men fewer MI’s, women more, overall increased rate of

HD 269 deaths in experimental group, 206 in controls Study unpublished for 16 years: “We were just disappointed in the way it came

out.” AHA- started recommending low-fat diets in 1961 NIH- called for a “definitive test” of the fat-cholesterol hypothesis in 1971

But ended up with two smaller tests That HD could be prevented with cholesterol-lowering drugs That HD could be prevented with cholesterol-lowering diet, smoking cessation, and BP

meds Neither of these actually tests the hypothesis

The Official Story Advances AHA- now everyone recommended low-fat diet- 1970

Not just high-risk men with past MI, high chol, or smoking hx And AHA seen as main source of expert info

1970’s- polyunsaturated fats assoc with CA in animals So advice to eat less fat and less saturated fat

1977- Dietary Goals for the US- now government says eating less fat helps health

Staff director Marshall Metz: “We really were totally naïve, a bunch of kids who just thought, Hell, we should say something on this subject before we go out of business.”

55-60% carbs, fats from 40% to 30%, only 1/3 saturated- the official diet They admit there’s no evidence that lowering dietary fat lowers blood chol,

but justify it with weight loss “Fat supplies 9 calories per gram, whereas protein and carbohydrates …

supply only 4 calories per gram. … Consequently, … the consumption of a diet deriving 40 percent of its calories from fat may result in a continual struggle to lose weight.”

So… USDA Dietary Guidelines for Americans “Avoid Too Much Fat, Saturated, Fat, and Cholesterol”

And (in NEJM), “To be a dissenter was to be unfunded because the peer-review system rewards conformity and excludes criticism.”

NHLBIstudies

Multiple Risk Factor Intervention Trial (MRFIT) 12K men with chol >290 Half advised to quit smoking, take BP meds, eat low-

fat, low-chol diet 7 years later, more deaths in experimental group

Lipid Research Clinics (LRC) Coronary Primary Prevention Trial

3800 men with chol >265 All told to eat chol-lowering diet, half given chol med 71 deaths in control group, 68 in experimental So… Keys was right, and lowering chol saves lives (?)

“It is now indisputable that lowering cholesterol with diet and drugs can actually cut the risk of developing heart disease and having a heart attack.”

But- extrapolation from drug study to diet Now- massive health campaign

The LRC results “strongly indicate that the more you lower cholesterol and fat in your diet, the more you reduce your risk of heart disease.”

AHA president: “If everyone ate chol-lowering diet, “we will have [atherosclerosis] conquered” by the year 2000

4 other studies, 1980-84, trying to establish a relationship btw dietary fat and health- none succeeded

And low cholesterol levels found to be associated with higher risk of CA- many studies (p. 54 GCBC)

NHLBI: “Surprise and chagrin” But- NIH “consensus conference” to establish

unanimity Held in 1984, interestingly…

Note: All page references are to Gary Taubes’ Good Calories, Bad Calories

Getting the Word Out1988- Surgeon General’s Report on Nutrition and

HealthThe “disproportionate consumption of food high in

fats” now responsible for 2/3 of the 2.1 M US deaths in 1988

“The depth of the science base… is even more impressive than that for tobacco and health in 1964.”

National Academy of Sciences- Diet and Health“Highest priority is given to reducing fat intake,

because the scientific evidence concerning dietary fats and other lipids and human health is strongest and the likely impact on public health the greatest.”

The media reports it, and now the debate is about low-fat vs. very low-fatHow much fat do we need to cut out in order to be

healthy?

The Fat-Cholesterol HypothesisLowering cholesterol prevents HD

Evidence ambiguous at best- statins, for example, work to lower chol and reduce MI’s, but the heart effect is probably more by reducing inflammation, like aspirin

Eating less fat or saturated fat lowers cholesterol and prevents HDEvidence ambiguous at best

And prolongs lifeEvidence ambiguous at best, diets may cause more harm

than goodAncel Keys, later in life

“No basis” to make the claim that trends in HD mortality reflect changes in diet

1987: “I’ve come to think that cholesterol is not as important as we used to think it was.”

Diseases of CivilizationTribal and indigenous populations tend to have low

levels of the “diseases of civilization”When exposed to Western diet- including sugar,

molasses, white flour, white rice- these diseases appearObesity, diabetes, CVD, HTN, stroke, CA, cavities,

periodontal dz, appendicitis, ulcers, diverticulitis, gallstones, hemorrhoids, varicose veins, constipation

When any of them appear, they eventually all doStress, other factors also important

The Carb Hypothesis: The dietary cause of these diseases is the consumption of refined carbohydratesRejected in the 1970’s- incompatible with fat-chol

idea

ReportsF.P. Fouche, South Africa, 1925, British Medical Journal

“I never saw a single case of gastric or duodenal ulcer, colitis, appendicitis, or cancer in any form in a native, although these diseases were frequently seen among the white or European population.”

Smithsonian Institution, 1908“Malignant diseases, if they exist at all… must be

exceedingly rare.”As were CVD, appendicitis, peritonitis, ulcer, etc.The Native Americans (SW US and Mexico) lived as long

as or longer than local whitesIsaac Levin, Columbia U, 1910- survey of 107

physiciansBuchanan- 15 yr practice, 2000 Indians, avg lifespan 55-

60, one case of CAGoodrich- 13 years, 3500 Indians, zero cases of CATotal- 115,000 Indians, treated for a few months to 20

years, 29 total cases of malignant tumor

Early StudiesThe Natural History of Cancer, 1908

Many continents and regionsFiji- 120,000 tribal people, 2 deaths from CABorneo- Dr. Pagel- 10 years, zero cases of CAIn NYC, 32 deaths per 1000 people in 1864, 67

in 1900 Philly- 31 in 1861, 70 in 1904

“The negative evidence is convincing that in the opinion of qualified medical observers cancer is exceptionally rare among primitive peoples”Fredrick Hoffmann, later a founder of the ACS

Why is this?Paleolithic diet high protein (19-35%), low carb

(22-40%), high fat (28-58%) in one estimateCarbs, especially refined carbs (cereal grains,

dairy, drinks, veggie oils, sugar, candy), are over 60% of calories in modern diet, but virtually absent in Paleo

White flour and sugar increase in late 19th century in Western diets right along with the rise in CA mortality (and DM, appendicitis, etc)

Stress levels also a factor- assoc with hierarchyWestern diet and higher stress levels are both

aspects of hierarchical society

Refined CarbsThe more refined, the whiter

The lower the vitamin, mineral, protein, and fiber This is why enriched flour has to be enriched

But- “more attractive to the eye” Better baking properties Bran (and molasses) sold for livestock and industry Better “digestibility” (i.e., a higher glycemic index) Less liable to infestation (!)

Mid-19th century- technological advances White flour less expensive- invention of roller mill Sugar less expensive- sugar-beet cultivation spread

White rice- mechanical rollers mid-20th century And we like it! WWI England- 90 lbs. sugar per year- 500%

increase in a century- Americans 80 lbs.Refining carbs the most drastic dietary change since

agriculture

Metabolic SyndromeImbalances common to obesity, DM, CVD

Abdominal obesityElevated triglycerides and free fatty acidsLow HDL, high LDL (small, dense LDL)High blood pressureHyperinsulinemiaInsulin resistance/glucose intoleranceProthrombotic stateProinflammatory state- elevated C-reactive proteinElevated uric acid- precursor of gout

These predict each other and major disease outcomes

All worsened by refined carbsCA also- same incidence patterns, but not part of

syndromeAlso stress- elevated GC’s, epi, norepi in syndrome

Carb Hypothesis 1966- Cleave- diseases of civ- CHD, obesity, DM, ulcers,

appendicitis- all symptoms of an underlying saccharine disease Adding sugar, flour, and white rice to any diet leads to

chronic disease- same dz no matter the previous diet Dental caries the “canary in the coal mine”

Weston Price- dental dz correlates with diet Sugar and starch fed to different animals

Raised cholesterol, TG’s, insulin High-sugar diets to college students

Raised cholesterol, TG’s, insulin, blood cells stickier Sugar predicts HD mortality

1975- the higher the sugar intake (in several nations), the higher the incidence and mortality from CA of colon, rectum, breast, ovary, uterus, prostate, kidney, NS, and testes

Sugar responsible for the diseases of civilization Law of Adaptation- species require time to adapt to a new feature

in the environment Confound- an unaccounted-for variable in an experiment

Affluence- meat and fat consumption tend to go up, grains down along with total carbs, but refined carbs up, often drastically In US, 15# sugar/year in 1830’s to 100# by 1920’s and 150# by 2000

(including HFCS) Which one causes the chronic diseases?

What’s Wrong with Sugar? Homeostasis- the body tries to restore and maintain

balance Hormonal regulation- reproduction, growth, homeostasis,

energy metabolism Insulin- the dominant hormone in energy metabolism

Regulates fat, carb, and protein metabolism Chronically high in obesity Type I DM- emaciation, lack of insulin Type II DM- obesity, hyperinsulinemia, insulin

resistance- impaired ability to use blood sugar, but not to store it as fat

Glycemic index- rate of digestion, absorption, and conversion of carbs to blood sugar The higher the GI, the higher the blood sugar spike

And the higher the resulting insulin rise Glucose = 100 Fat and protein decrease GI, refined carbs raise it

So carbs, especially refined carbs, cause more rapid blood sugar spikes, leading to more rapid and pronounced elevations of blood insulin Leading to all sorts of nasty health effects!

Diabetes High blood glucose

Glycosuria, frequent urination Constant hunger for sugar and refined carbs Urine smells and tastes like sugar (DM aka “sugar sickness”)

Absent in isolated populations eating traditional diets Rise in type 2 DM inWestern societies coincides with rise in

consumption of sugar and white flour Death rate from DM up 400% btw 1900 and 1920 in US, up 15X

since Civil War, similar in Britain and France “Rises and falls in the sugar consumption are followed with fair

regularity within a few months by similar rises and falls in the death rates from diabetes.” -H. Emerson, Columbia U, 1924

Of the 13 countries highest in consumption of sugar, 11 are found among the 13 highest in death rate from diabetes

DM found in 0.1% of US population 100 years ago Now 7%, a 70-fold increase Mainstream view- DM from obesity, inactivity, and fat-rich low-carb

diet Elliott Joslin- Joslin’s Diabetes Mellitus- updated versions still

prominent today 1920’s- pioneered insulin as DM Tx- insulin discovered in 1921

HypertensionBP greater than 140/90Moves together with CVD, stroke, obesity, DM, high

triglyceridesMainstream- salt as the dietary cause of HTN

Water retained along with the salt, blood volume up But effect small- cutting salt intake in half lowers BP by <5

mm Hg- the body normally just excretes the salt Insulin elevated in HTN- an insulin-resistant state

Encourages the kidneys to hold on to sodium Stimulates the SNS, stress response

Increases HR, constricts blood vessels = higher BP Joslin’s DM: chronically elevated insulin “the major

pathogenetic defect initiating the hypertensive process” in type 2 DM

High blood glucose inhibits salt excretion, so we retain water And is itself a solute helping to retain water, just like salt

Carb Hypothesis- carbs raise insulin levels, leading to HTN, obesity, other diseases of civilization

Lipids and CVDFat- free fatty acids (the chains by themselves) and

triglycerides (three chains attached to glycerol)CholesterolLipoproteins

HDL- high-density lipoprotein- carries the “good cholesterol” The higher the better

LDL- low-density lipoprotein- carries the “bad cholesterol” The lower the better But there’s more to the LDL story!

VLDL- very low-density lipoprotein- carries triglycerides Also the lower the better

1950- ultracentrifuge fractionates lipoproteins LDL and VLDL can predict CVD, but atherogenic index combining both even

better Majority opinion- lipoproteins not important LDL elevated by saturated fats

VLDL elevated by carbs, so who’s the culprit? 1955- carbohydrate-induced lipemia

Test tubes- which one is cloudy? Joslin: “The percent of fat (in the blood) rises with the severity of the

disease (diabetes)… and is especially related to the quantity of carbohydrate, … rather than with the fat administered.”

1961- Elevated TG’s (associated with CVD risk) in 5% of healthy young men 38% of middle-aged men 82% of coronary patients

Low-fat, high-carb diets raise TG’s High TG’s much more strongly associated with CVD than high blood

cholesterol AHA embracing Keys hypothesis at the time

NIH doesn’t test lipoproteins until 1967 5 studies- results 1977

Total blood cholesterol not predictive of CVD LDL a “marginal” risk factor TG’s predict CVD HDL the strongest predictor of all

The higher the HDL, the lower the TG’s, and the lower the risk of heart disease HDL the largest impact, and the only good predictor for age >50

Lipids and CVD

What’s the Spin?NHLBI and AHA

Keep the science simple for the public Reconcile this with fat-cholesterol hypothesis

So… the effort shifted to lowering LDL cholesterol, not total cholesterol

2003- National Cholesterol Education Program): “Robust relationship between total cholesterol and (CVD)… implies that an elevated LDL is a powerful risk factor.”

A “marginal” risk factor becomes, using the same data, “powerful” and “significant”!

And of course, this implicates saturated fats, not carbsSince TG’s tend to move with obesity, DM, and HDL, and obesity is

caused by the high-fat diet, TG’s not important by themselves, so no need to focus on dietary carbs (!)

HDL and TG’s still the dominant predictors, though Dietary carbs lower HDL (and raise TG’s, and lower LDL) Saturated fats raise HDL and LDL Monounsaturated fats lower LDL, raise HDL

Oleic acid- the main fat in olive oilAdvice- lower HDL through exercise and weight loss

Low-fat, high-carb diets to lose weight Monounsaturated fats as the heart-healthy fats

Heart-Healthy BaconHaven’t you always wanted to hear that? Here

you go!Oleic acid also the main fat in meat, eggs, bacon,

lardA Porterhouse steak with ¼ inch layer of fat, for

example 51% monounsaturated, 90% of this is oleic acid 45% saturated

1/3 of this is stearic acid, which metabolizes to oleic acid 4% polyunsaturated- lowers LDL, no effect on HDL So- 70% of the fat in meat raises HDL and lowers LDL,

while the other 30% will raise HDL and LDL And that 30% gets a clean bill of health also- read on!

LDL Subtypes1980- 7 subtypes of LDL

Smallest, densest LDL- strong negative correlation with HDL Elevated in CVD

Squeezes more easily through damaged artery walls Structural changes in protein facilitating adhesion Remains in bloodstream longer Oxidizes more easily

LDL in the population in two patterns Pattern A- large, fluffy LDL, low CVD risk Pattern B- small, dense LDL, high CVD risk

High TG’s, low HDL (not in pattern A) This pattern (the atherogenic profile) also found in DM

The higher the dietary carbs The smaller and denser the LDL The more likely the appearance of pattern B The greater the CVD risk

The more saturated fat in the diet, the larger and fluffier the LDL!

Carbs and CVDSo dietary carbs now elevate TG’s, lower HDL,

and, although they lower total LDL, raise the small, dense LDL that’s associated with CVDAnd saturated fat raises the large, fluffy, and

harmless LDL!Insulin- the higher the levels, the greater the CVD

Stimulates TG synthesis and secretion to fat cells Insulin resistance exacerbates this

Enhances transport of cholesterol and fat into the arterial wall

Stimulates chol and fat synthesis in artery wallEnhances smooth muscle cell proliferation in artery

walls

Sugar ToxicityReactive oxygen species- burning glucose transforms

oxygen into free radicals and other oxidants – oxidative stress Free radicals- assoc with CVD, CA, others

Change cell membrane permeability Harm mitochondria Inhibit DNA coding Distort RNA communication

Neutralized by antioxidantsAdvanced glycation end-products (AGE’s)

Glycation- sugar attaches to protein without enzyme Random reaction, leading to more of same

The sugar disengages in low blood sugar In high blood sugar, continuing process = AGE’s

AGE’s cross-link with each other and other proteins Accumulate in eye, kidney, arterial lining, nerve endings

All of which are damaged in DM Collagen- most abundant protein, structural

AGE version ages skin- diabetics look older Also stiffening of joints, arteries, heart, lungs- leather

Sugar and CVDLDL particularly susceptible to glycation

As is HDL, making them both more atherogenicLDL also susceptible to oxidation

Trapped in artery wall more effectively, along with its cholesterol, and more resistant to removal from blood

Elevated in CVD patients, particularly in the plaquesSucrose- table sugar

Glucose and fructose, split and metabolized separately Resulting in effects on insulin levels, the direct

effects of glucose, and the health effects of fructose Sucrose and HFCS the worst of both worlds- p. 201

FructoseFructose-induced lipogenesisFructose stimulates TG synthesis in liver

Fructose also blocks glucose metabolism in the liverAnd glycogen synthesisSo more insulin secretedFructose-induced HTN greater than glucose

Fructose way more reactive in AGE formation than glucoseAnd 10x more effective at cross-linkingAnd the AGE’s and cross-linked proteins more resistant to

degradationFructose greatly increases the oxidation of LDL’s, tooTwo enzymes (acyl-CoA and acyl-carnitine) suppressed

by fructose- this tells cells to store fat, not burn itFructose increases pyruvate dehydrogenase (PDH,

another enzyme) synthesis in liverCells burn sugar, not fat- metabolism skewed toward fat

storageFatty liver disease, like in alcoholics

High Fructose Corn Syrup HFCS-55- 55% fructose, 45% glucose

Introduced in 1978 Cheaper substitute for sugar in US

Corn subsidies and sugar tariffs Lower cost encourages consumption

Liquid- easier to blend and transport “Fruit sugar,” so it must be natural…

US- 110-120# of caloric sweeteners per capita per year Up in 1960’s, coinciding with HFCS precursors 124# sugars 1975-79 150# in 2000, almost completely due to HFCS Paralleling the rise in obesity

HFCS soft drinks 10x richer in carbonyl compounds than diet soda control Involved in AGE formation Elevated in diabetics and implicated in foot ulcers, retinopathy,

neuropathy HFCS induces leptin (satiety signal) resistance

People keep eating and don’t feel full- hungry ghosts! HFCS tainted with mercury- 1/3 of products tested

Mercury made the Mad Hatter mad! Caustic soda and HCl used in HFCS production

Fructose and HFCSContinuing systemic denial

Several studies: HFCS no different than other energy sources Funded by American Beverage Institute, Corn Refiners Association

"I don't think there should be a perception that high-fructose corn syrup has caused obesity until we know more.“-Dr. Barry M. Popkin

"There's no substantial evidence to support the idea that high-fructose corn syrup is somehow responsible for obesity .... If there was no high-fructose corn syrup, I don't think we would see a change in anything important.“ Walter Willett, Harvard School of Public Health, Nutrition dept

chair"Doubt is our product since it is the best means of

competing with the 'body of fact' that exists in the mind of the general public."1969 memo written for cigarette maker Brown & Williamson

“It is difficult to get a man to understand something when his salary depends upon his not understanding it.” Upton Sinclair

Cancer At least 75-80% preventable with diet and lifestyle

Some role for pollution and chemicals Diet the largest role

Increasing incidence in CA GI- colon, rectal, gall bladder Endocrine- breast, endometrial, ovarian, prostate These are the cancers related to diet and lifestyle

Incidence patterns similar to CVD, DM, obesity Another disease of civilization

Sugar intake correlated with incidence and mortality In colon, rectal, breast, ovarian, prostate, kidney, nervous system,

and testicular CA 5 countries with highest sugar intake also the 5 countries with the

highest breast CA mortality 5 lowest = 5 with least mortality

Tumors burn much more sugar than normal cells CA linked to glucose intolerance

Cancer

Insulin Acts a growth promoter,

normally and in CA Fuel and growth signals to

cells, including CA cells Breast CA tumors- more

receptors for insulin IGF- insulin-like growth factor

Prominent hormone in growth regulation

Also elevated in high-carb diet Can mimic effects of insulin,

and vice versa Levels of both tend to move

together over time IGF enhances tumor growth

IGF receptors necessary for tumor growth Particularly with estrogen

Tumors can secrete their own IGF

Tumor cells have more IGF receptors

Insulin unbinds IGF to enter cells

IGF also overrides the cell suicide program

Insulin and IGF both cause benign tumors to metastasize

They accelerate the process of the cell becoming cancerous, and keep it alive and multiplying

Hyperinsulinemia and elevated IGF in breast, prostate, colorectal, and endometrial CA

So the carbs lead to extra insulin and extra blood sugar along with extra IGF and extra signals to proliferate

They don’t cause the CA, but they encourage the transformation into malignancy

An ideal environment for CA growth

Alzheimer’s DiseaseProgressive and fatal brain diseaseMost common form of dementiaPlaques- beta-amyloid protein between cellsTangles- protein inside dying nerve cells

Both disrupt nerve cell communicationBoth accumulate in most people

Risk factors- age, genetics, family history, smokingAlso- HTN, CVD, stroke, DM, metabolic syndrome

Hyperinsulinemia tooAnother disease of civilization

Incidence patterns similar to CVD, DM, obesity2x increased risk in diabetics

4x if on insulin

Alzheimer’s DiseaseAmyloid- normal protein in

brain Healthy brains clear it out,

but not in AD AGE’s found in plaques and

tanglesNobody knows for sure what

causes ADTheory- AD starts with

glycation Proteins stick to

themselves and each other Disposal mechanisms don’t

work, so they accumulate Cross-linking leads to AGE’s Glycation also generates

ROS (free radicals) Damaging neurons further

Insulin-degrading enzyme (IDE)

Clears both amyloid and insulin

Insulin can monopolize it In animals- the less IDE

available, the more amyloid Mice without IDE gene get

AD and type 2 DM Insulin given to healthy

elderly volunteers Amyloid increased proportionately The older the person, the greater

the increase Decreasing insulin increases

amount of IDE

Obesity

The Official Story- weight gain comes from taking in too many calories and/or expending too fewSurgeon General: “Overweight and obesity result

from excess calorie consumption and/or inadequate physical activity.”

US, 1970’s to 1990’s: increased caloric intakeNHANES- 1971 to 2000- 150 calories per day in

men, 350 in womenUSDA- 1971 to 1982: 3300 calories per day per

person 1993-1997: 3800 calories 90% of the 500 calories from carbs

The rise in obesity also coincides with increasing exercise

The Pima Indians Highest rates of obesity and diabetes in the US

Is it their genes? NIH: “If the Pima Indians could return to some of their traditions,

including a high degree of physical activity and a diet with less fat and more starch, we might be able to reduce the rate, and surely the severity, of unhealthy weight in most of the population.” (If we’re trying to fix it, then surely we didn’t help cause it in the first place! And we’re certainly not just going to give them back the land and the water we took…)

Early 19th century and before Game, fish, clams, corn, beans, cattle, poultry, wheat, melons, figs,

cactus 1846: “Sprightly… in fine health… the greatest abundance of food”

1860’s: “Years of famine” as white and Mexican settlers came in Game hunted nearly to extinction, water taken by the whites

1890’s: government rations to avoid starvation 1900’s: “Real obesity is found almost exclusively among the Indians

on reservations” The rations- 50% of calories from sugar and flour

1950’s: “large quantities of refined flour, sugar, and canned fruits high in sugar,” also soda, candy, chips, cakes

1962: “soda pop is used in immense amounts”

The Official Story Energy Balance and the First Law of Thermodynamics

A calorie is a calorie is a calorie Change in energy stores = energy intake – expenditure

Weight gain accompanied by positive energy balance- eat more than you burn, and you get fat

Obesity causes or worsens the conditions of metabolic syndrome and the diseases of civilization And obesity caused by overeating, particularly a high-fat diet, and

inactivity, so low-fat diet and exercise to fix “Willful descent into self-gratification”

The obese responsible for their condition Character defect- they overeat and won’t change Willpower is the cure

Like alcoholism from overdrinking Assumption- intake and expenditure are independent variables

We can change one without changing the other USDA- “For most adults a reduction of 50 to 100 calories per day

may prevent gradual weight gain.” Low-fat, high-carb diets and exercise recommended for weight loss

Fats fatten us the most effectively (in this view)

Tale of the Tape- Low Cal DietLow-cal semi-starvation diets

“Balanced” diets with fewer calories- calorie restriction

Benedict 1917 2 groups of 12 men, 1400-

2100 calories per day, 3 mos

Weight loss Constant hunger, feeling

cold Metabolism slowed 30% Anemia, weakness, loss of

concentration, loss of libido Weight gain on any more

than 2100 cals Binge eating after study, all

weight regained in 2 weeks And another 8 lbs extra in the

next 3 weeks In general- 25% lost 20 lbs,

5% lost 40 lbs Almost all gained it back

Keys 1944 32 male conscientious

objectors 24 weeks on “semi-

starvation” diet- 1570 calories 400 cals protein, 270 fat, 900 carbs Also 5-6 mile walk each day 12 lbs lost in 12 weeks Another 3 the next 12 weeks Slow nail growth, hair loss,

increased wound healing time, metabolism down, slowed reflexes, depression, irritability, feeling cold

Constant hunger, fixation on food, cheating on diet

When allowed to eat, 8000 cals per day

Total weight gain 10 lbs

Tale of the Tape- Exercise Exercise-Jean Mayer, 1950’s- inactivity causes obesity

But correlation is not causation Two questionable studies, one on animals and one on humans,

never replicated “J. Mayer has since demonstrated, in both animal and human studies…”

-J. Mayer Björntorp 1973- 7 subjects, 6 months of exercise three times a

week, no change in weight Pi-Sunyer 1989- weights can go up, down, or remain steady Denmark 1989- sedentary people trained to run marathons for 18

months 18 men lost 5 lbs, 9 women lost no weight

Randomized trials show less effect Somewhere between 3 ounces a month gained and 2 ounces a

month lost Animal experiments- the more the rats run, the more they eat,

weights unchanged In hamsters and gerbils, voluntary running produced increases in

body weight and body fat Hunger and intake increase in proportion to the calories expended

“Working up an appetite”

What Makes Us Fat? To fatten- excess calories have to be stored as fat

Not stored as muscle, not burned in metabolism or physical activity

Continuing excess calorie consumption Massa tribe- Cameroon- fattening ritual

Normally- milk as staple, 2500 calories per day To fatten- milk with sorghum porridge, 3500 cals/day Typical gain 15-20 lbs. Fattening by adding carbs

Sumo wrestlers Normal Japanese diet 2300 cals/day Upper group- 5500 cals/day, 57% carbs, 16% fat Lower group- fatter, less muscular

5100 cals/day, 80% carbs, 9% fat Overfeeding studies- 10,000 calories of mostly carbs a day, but

hunger late in the day And exercise is controlled for- this is not just people eating a lot

because they’re elite athletes or otherwise exceptionally physically active- this is people eating 10,000 calories and still being hungry with normal activity levels

What Makes Us Thin? AHA- carb restriction today is a “fad diet”

But this was the standard medical treatment for obesity through most of the 20th century- p. 314

The AHA recommended high-carb, low-fat diets for CVD in the 1960’s, then for obesity, then for everybody, and low-carb diets were (and are) marginalized JAMA and Lancet: “Freak Diets!” (p. 331)

In the medical and nutritional mainstream, low-carb diets are considered freakish, dangerous, and unscientific. Keeping in mind the inability of science to demonstrate long-term, effective weight loss with the calorie-restricted low-fat “balanced” diet, let’s look at how the low-carb diet does.

V. Stefansson- early 20th century Lived with the Inuit for 10 years eating only meat

He and the Inuit were vigorously healthy So is the Inuit diet “balanced?” What does it mean for a diet to be

balanced? 1928- Stefansson and Anderson

Ate only meat for an entire year 79% fat, 19% protein, 2% carb (glycogen in muscle)

Ketone bodies in urine to rule out carb cheating Both in good condition afterward

6 and 3 lbs weight loss, BP decrease, no kidney damage, no gout, no vitamin or mineral deficiencies, a case of gingivitis cleared up

Tale of the Tape- Low-Carb Diet Denmark 1936

21 obese patients, 2 years 1850 calories/day, 25% carbs, 60% fat

Cream, butter, olive oil, eggs, cheese, meat 2 lbs weight loss per week, no chronic hunger or fatigue

Donaldson 1920’s: 6 oz meat, 2 oz fat, at each meal, no sugar, flour, alcohol, starch, ½ hour walk

17K patients, 2-3 lbs/wk loss, no hunger Alfred Pennington- DuPont 1949: 20 execs, 9-54 lbs loss, 2 lbs/wk, no

hunger, increased physical energy and sense of well-being No calorie restriction- min 2400, avg 3000 Carbs restricted to 80 cal/meal

Thorpe 1957- rapid weight loss (6-8 lbs/mo), no hunger, weakness, lethargy, or constipation

Ohlson and Young 1952: 14-1500 cals/day, 24% protein, 54% fat, 22% carbs 7 women, overweight to obese, 16 weeks, 19-37 lbs lost

No hunger, addition of muscle mass 16 overweight women, 9-26 lbs lost in 10 weeks, no hunger, “unexpectedly

healthy,” sense of well-being 8 overweight male students, 1800 cals/day, 9 weeks, 13-28 lbs lost, almost 3

lbs/week Leith 1961: 48 patients who had tried and failed with low-cal diets, 28 lost

btw 10 and 40 lbs “The patients ingested protein and fat as desired”

The Low-Carb DietWilder 1930’s: a few hundred cals/day, meat, fish, egg white,

80-100 cals of green veggies- weight loss without hungerBistrian 1970’s: 700 patients, 50% fat, 50% protein, 650-800

cals/day, weight loss without hunger1000, 1200, 1320, 1400, 1800, 2200, 2700, or no calorie

restriction at all- weight loss without hungerKemp 1956: low-carb diet, no calorie restriction

1450 overweight and obese patients 49% lost at least 60% of excess weight- 25# after 1 year 38% defaulted, 13% didn’t lose weight

Carb restriction usually does a lot better than low-cal “balanced diet” when compared directly, even when the low-carb diet has more calories- p. 337

6 recent trials- weight loss after 3-6 mos was 2-3x greater on low-carb, calorie-unrestricted diet than on calorie-restricted, low-fat diet

JAMA 2003: “Greater weight loss than higher-carbohydrate diets” 37# vs. 4#, p. 339

Glucose and the BrainConventional wisdom- “balanced diet” the best

Need carbs for brain glucoseAnd to prevent deficiency diseases

The brain runs mainly on glucose130 grams of carb considered the “minimum safe

levels”But if there’s less than 130 g, the liver makes

ketone bodies to supply brainAnd if no carbs at all, 75% of CNS fuel from ketones

The rest from glucose made from amino acids or glycerol Protein from diet or muscle

Ketosis- normal- 5-20 mg/dl in 5-10% carb diet Diabetic ketoacidosis- pathological- 200 mg/dl

DeficiencyDiseases

Studies all done with high-carb diets low in meat and dairy- p. 321

Meat contains all essential amino acids And 12 of 13 essential vitamins All in large quantities and in high-utility forms

Vitamin C- only small amounts in meat So scurvy can be cured by adding fruits and veggies But this doesn’t mean that the lack of these causes it! Inuit- no fruits, no veggies, no scurvy Carbs, esp refined carbs, increase our need for vitamins!

They flush out the vitamin C and inhibit its use Vitamin C deficiency as a disease of civilization

Deficiency diseases in general as diseases of civilization Scurvy from absence of fruits and veggies, or presence of

refined carbs?

Scurvy- vitamin CPellagra- niacin (vit B3)Beriberi- thiamine (vit

B1)Rickets- vitamin DAnemia- iron, vit B12,

folate

So What’s Going On Here? Official story- obesity from too many calories in, too few calories out

So eat fewer calories or exercise more to lose weight These are independent variables- you can change one without affecting the

other Obesity is a character defect- driven by the brain- and losing weight

is a matter of willpower, of overcoming the body But it doesn’t work!

Restrict calories, and activity and metabolism decrease Exercise more, and work up an appetite!

“Consistently high or low energy expenditures result in consistently high or low levels of appetite.” -Hugo Rony, 1940

1998: “Energy intake can be interpreted as a crude measure of physical activity.”

Carb Hypothesis- calories in and calories out are dependent, linked variables determined by a set point Any increase in energy expenditure induces hunger and increase in

intake Any decrease in intake induces decrease in expenditure

Slower metabolism or reduced activity Homeostasis- our bodies minimize long-term fluctuations in energy

reserves and maintain a stable weight, unless the set point is changed

HomeostasisSet points in the body for temperature, pH, blood

oxygen and CO2, blood pressure, etc.Regulated by hormones, as is body weight!

Positive caloric balance in children- eating because they’re growing- hormone-driven

Weight gain in pregnancy hormonal Height genetic and driven by hormones Fat distributed differently in men and women

All of these induce a positive caloric balance- the hormone levels change, and the set point changes with it This causes increased calorie intake, reduced expenditure

Carb Hypothesis- the same metabolic imbalance that drives us to fatten also causes metabolic syndrome and the diseases of civilization

What If It’s in the Body?1950’s- Pennington- what if energy balance is regulated in

the cells, by hormones, and not in the brain, by the ego? The less fuel for our cells, the greater the hunger and the

less energy expended The more, the greater the metabolic and physical activity Energy expenditure is an index of cellular calorie nutrition

The obese exist in energy balance also- “static phase” Body weight isn’t jumping around all over the place all the time;

there’s a stable, but higher, set point First law of thermodynamics, but now applied not to the

whole body, but to the fat deposits If energy goes into the fat tissue faster than it comes out, weight

gain results Less energy for cells, greater hunger and lethargy Until the fat cells get full (like balloons), and a new steady state is

reached Fat cells in the obese hold on to fat more strongly

The obese are sedentary because their fat cells are holding on to fat instead of burning it- the cells are semi-starved

Metabolic imbalance, fixed by carb restricting

Cellular NutritionSo then, if the fat cells are holding fat too tightly,

low-calorie diets would just starve the cells furtherHunger, decreased metabolism and activity- as we see!

If low-carb diets correct the metabolic imbalance, then fat can flow freely out of the fat cells againNew equilibrium btw energy storage, intake, and useFat deposits would shrink- energy stores finally being

used!Decreased appetite as more energy available from body

fat Not because the diet is boring Eating less because fat tissue shrinking, not fat tissue

shrinking because eating lessNegative energy balance as energy supplied from body

fatIncreased metabolism, physical activity

Cells no longer starving

So What’s the Imbalance?Official story- there is no imbalance- fat is evil and

carbs are the cure- willpower is the problemJAMA 1955: The “theories that attributed obesity to

an endocrine disturbance have been shown to be erroneous.” Good thing that’s all cleared up, 5 years before insulin could

even be measured in the blood and another few years before obesity was associated with hyperinsulinemia and insulin resistance!

Carb Hypothesis1. Obesity caused by an imbalance in fat metabolism2. Insulin plays the primary role in fat metabolism3. Carbs, particularly refined carbs, and especially

fructose, elevate insulin levels and resistanceThe carbs are the primary cause of common obesity

Carbs in the diet spike blood glucose, leading to hyperinsulinemia

Insulin Signals the “fed state” in the body- sends energy from blood to fat, muscle,

and organ Secreted in response to increases in blood glucose- tells body that carbs are

abundant Tells the body to store nutrition as fat

Increases conversion of glucose to fat Increases adipose receptivity to circulating fat Increases fatty acid storage and conversion of other foods to fat

The principal regulator of fat metabolism- p. 391 Glucose into fat cells, formation of glycerol, etc.

Insulin low = lipolysis, fat loss Insulin high = lipogenesis, fat accumulation Several hormones mobilize FFA, but insulin and blood glucose suppress them

all Insulin injected into diabetic dogs or humans causes hunger, weight gain, body

fat deposition Used to fatten anorexics and underweight children Appetite specifically for carbs The carbs then stimulate insulin production- vicious cycle Insulin resistance creates another vicious cycle

“Carbohydrate is driving insulin is driving fat” Fat cells hypersensitive to insulin

Even low levels of insulin shut down FFA outflow And fat cells remain sensitive to insulin long after muscle cells aren’t anymore

Insulin and Weight The body regulates fuel flow to the cells

Body fat accumulation is a secondary effect Anything that elevates insulin will

Deposit fat in the fat tissue Inhibit FFA mobilization Promote weight gain and hunger Lowering insulin promotes FFA release, satiety, and weight loss

Weight gain comes from insulin elevation Hunger lengthened, satiety shortened Fat deposits unavailable Cells signaled to burn glucose- p. 436

The body will burn carbs when there are high blood sugar, full glycogen stores

As reserves tapped or greater energy demanded, FFA from fat cells take up the slack

All dietary fat and some of the carbs stored as fat 50-70% of our daily energy

Hunger, satiety, and taste driven by metabolic needs and physiological conditions at the cellular level

It’s in the body, not the brain! Caloric homeostasis- we eat to maintain the flow of energy to cells

Cellular nutrition is a higher priority than the size of the fat stores

Two Situations So here’s how the high-carb situation looks:

Carbs raise blood sugar raises insulin The insulin tells the body to store nutrition as fat There’s a burst of energy after a high-carb meal as the muscles

and organs get sugar But then, as the insulin tells the body to store energy, and as the

sugar runs out, the fat that could power the cells can’t be released The muscle and organ cells become depleted Creating hunger and carb cravings (and sayings about being

hungry an hour after eating Chinese food, not that Western high-carb meals don’t do the same)

And another round of carb intake This vicious cycle continues until the fat cells are full

A new steady state at a higher weight Weight only plateaus when

The fat tissue becomes insulin-resistant Or the increased concentration of FFA’s in the fat cells or other

forces balance out the insulin This is determined by individual variation in carbohydrate

sensitivity

Two SituationsAnd here’s the low-carb situation:

Blood glucose and insulin are not chronically elevatedSo after a low-carb meal, they stay lowThe muscle cells fill with energy, and the rest is stored

as fatBecause the insulin is low between meals, the stored fat

is easily accessible and freely releasedThe cells draw on this reserve to stay well nourishedWhen the reserves run low (several hours later, not an

hour), the body (not the brain, the cells!) signals hungerEat another low-carb meal and start the process againAt no point does fat accumulate in the fat cells, so at no

point do weight gain and obesity developAnd because glucose and insulin stay low, they aren’t

able to drive the other diseases of civilization either

Testing the Models Mainstream predictions for the high-carb diet

Radiant health, lean physique, easy weight loss through calorie restriction and exercise, obesity as a character defect

Being free of the demon of fat makes for a life of vibrant health and happiness

Carb hypothesis predictions for the high-carb diet Persistent hunger, even with high calorie intake Weight gain and obesity Inability to achieve lasting weight loss- rebound weight gain Hunger, decreased metabolism, and inactivity while trying Increased appetite with exercise The chronic diseases of civilization

Scientific data for the high-carb diet Persistent hunger, even with high calorie intake Weight gain and obesity Inability to achieve lasting weight loss- rebound weight gain Hunger, decreased metabolism, and inactivity while trying Increased appetite with exercise The chronic diseases of civilization

Testing the Models Mainstream predictions for the low-carb diet

Weight gain, obesity, heart disease, the other diseases of civilization The excess calories in fat prevent weight loss Deficiency diseases, gout, kidney damage, ketosis and possible brain

damage Unscientific Freak Diets

Carb Hypothesis predictions for the low-carb diet Radiant health, lean physique, easy weight loss through carb restriction Satiety between meals, easy access to fat stores Weight loss without hunger, decreased metabolism, inactivity, or

rebound weight gain Relative absence of the diseases of civilization

Scientific data for the low-carb diet Radiant health, lean physique, easy weight loss through carb restriction Satiety between meals, easy access to fat stores Weight loss without hunger, decreased metabolism, inactivity, or

rebound weight gain Relative absence of the diseases of civilization

(Note- these last two slides are a little tongue-in-cheek, but the preponderance of evidence, scientific and otherwise, supporting the carb hypothesis is overwhelming.)

Stress Effects Stress and Nutrition

GC’s stimulate appetite And preferentially for starch,

sugar, and fat Make brain less sensitive to

satiety signal (leptin) Particularly in the case of

frequent intermittent stressors (also known as normal days in modern culture!)

Synthesis of cortisol depletes nutrients- vitamins and minerals Caused/exacerbated by simple

sugars Increased cortisol increases

neuropeptide Y Carb cravings

Stress hormones shunt energy into the blood TG breakdown, FFA and glycerol

flood the circulation Proteins to amino acids to

glucose Increased LDL, decreased HDL

Caffeine, processed sugar, processed flour, and salt elevate the stress response

Stress and Type 2 DM Stress promotes insulin

resistance Fat cells less sensitive to insulin in order

to shunt energy to muscles Increases autoimmune attacks on

pancreas Increased FFA, glucose in blood Stress and Addiction Using the drug decreases stress

during the buzz The stress comes in as the effects wear

off Increases likelihood of addiction Increases extent of addiction Increases difficulty of withdrawal Increases likelihood of relapse Grains contain exorphins Opioids like morphine or heroin, and also

addictive Sugar and refined carbs stimulate the

same dopamine pathways as addictive drugs

Apples and PearsPear shape- gluteal fatApple shape- abdominal fat- worsened by stress

Greater risk for CVD, DM, other dz of civGC’s promote apple obesity in the presence of high

insulinAbdominal fat cells more sensitive to GC’sAbd fat released straight to liver

Converted to glucose, elevated blood sugarStress -> carb cravings -> apple obesity -> dz of civThe carbs and the apple fat both reduce the stress

response- they really do help you feel good, as addictions doUntil the insulin stores the carbs as fat, starving the

muscle cells and creating stress, starting the cycle over again

Also, lower ranking humans are more likely to be obese and more likely to be apple obese

Digging at Roots

Obesity is found only in humans and domesticates, not wild animals And it’s associated with the Western diet So what are we doing that the other animals aren’t?

Among other things, no other animals grow grains As we changed our diet to first increase carbs (agriculture),

then refine them (industrialization), we disrupted our homeostasis Increasing blood sugar, blood insulin, insulin resistance And creating imbalance in our bodies, as well as the land, our

psyches, and our social relationshipsAlong with agriculture and the dawn of civilization,

Nutrition worsens Lifespan and body stature decrease Famine, anemia, rickets, epidemic infectious disease The Diseases of Civilization (no surprise, right?) Work increases sharply As does environmental destruction And social hierarchy And chronic stress

Food Issues RevisitedIndustrial agriculture

GMOsPesticides/chemicalsOther environmental effectsSweatshops and hierarchy/slavery

Factory farming and animal treatmentEnvironmental effects

Food addictionInstitutional reality

CorporationsGovernments

Domestication and the energy of foodWaste- 25%In the end, no one right way to eat

Your body knows how to eat. Your Primal Matrix knows- listen!

What do these all have in common? What’s the underlying relationship?