Body FunctionsDIMS

Summer 2013

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%

Conventional WisdomHow 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 plaques

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

Increase in cancer incidence also during this period Inflammation? Toxins? Carbohydrates? Maybe any or all, or

something else, but evidence against dietary fat as the cause

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

Metabolic Syndrome

Imbalances common to obesity, DM, CVDAbdominal obesityElevated triglycerides and free fatty acidsLow HDL, high LDL (small, dense LDL)HypertensionHyperinsulinemiaInsulin resistance/glucose intoleranceProthrombotic stateProinflammatory state- elevated C-reactive proteinElevated uric acid- precursor of goutAlso- endothelial dysfunction, oxidative stress,

inflammationRelated- polycystic ovary syndrome, fatty liver disease,

erectile dysfunctionThese predict each other and major disease

outcomesMany worsened by refined carbs and stress

CA also- same incidence patterns, but not part of syndrome

Also stress- elevated GC’s, epi, norepi in syndrome24% of US adult population

Glycemic Index 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 Glycemic load- GI per portion

Recent studies- diets high in GI, GL, starch assoc with increased DM risk Low-GI diets assoc with improved glycemic control, insulin sensitivity Total dietary fat not a risk factor for type 2 DM

So carbs, especially refined carbs, cause more rapid blood sugar spikes, leading to more rapid and pronounced elevations of blood insulin

Sugar Toxicity Reactive 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 antioxidants Advanced 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

LDL particularly susceptible to glycation As is HDL, making them both more atherogenic

LDL 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 plaques

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 in Western 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

Obesity and diabetes Fat cells distend and respond less to insulin Less glucose and fat taken up- CV damage Hormones then trigger fat and muscle to become more insulin-

resistant Pancreas secretes more insulin Vicious circle, leading to beta cell burnout and type I DM

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

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

Building the Official Truth 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 Keys: “The peculiarities of those primitive nomads have no relevance to

diet-cholesterol-CHD relationships in other populations.” 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 association 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

“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.” 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.”

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

would support the hypothesis

The OfficialStory 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 “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 Out

1988- 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?

1955- Ahrens- carbohydrate-induced lipemia Test tubes- “The lipemic plasma was

obtained during the high-carbohydrate period, and the clear plasma during the high-fat regimen.”

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.”

Dietary carbs elevate TG’s, lower HDL, and, although they lower total LDL, raise the small, dense LDL that’s associated with CVD

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 wall Enhances smooth muscle cell proliferation

in artery walls

Carbs and CVD

LDL Subtypes1980- 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

Small, dense LDL- Elevated in CVD Strong negative correlation with HDL Squeezes more easily through damaged artery walls Structural changes in protein facilitating adhesion Remains in bloodstream longer Oxidizes more easily

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!

Cancer Increasing CA incidence

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

At least 75-80% preventable with diet and lifestyle Some role for pollution and chemicals, genetics Diet the largest role

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 (apoptosis) 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 may not cause the CA, but they encourage the transformation into malignancy

An ideal environment for CA growth

Alzheimer DiseaseMost common form of dementia

Progressive and fatal brain diseasePlaques- 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,

hyperinsulinemiaAnother disease of civilization

Incidence patterns similar to CVD, DM, obesity2x increased risk in diabetics, 4x if on insulin

Alzheimer 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

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

Obesity

F.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 whites Isaac Levin, Columbia U, 1910- survey of 107 physicians

Buchanan- 15 yr practice, 2000 Indians, avg lifespan 55-60, one case of CA Goodrich- 13 years, 3500 Indians, zero cases of CA Total- 115,000 Indians, treated for a few months to 20 years, 29 total cases

of malignant tumor Low levels of CA, CVD, etc., among:

Inuit eating all-meat diet Masai eating blood, milk, and meat

The Natural History of Cancer, 1908 Many continents and regions Fiji- 120,000 tribal people, 2 deaths from CA Borneo- Dr. Pagel- 10 years, zero cases of CA In 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

Reports

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.”

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

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.” Calorie-restricted, low-fat, high-carb diets and exercise

recommended for weight loss Fats fatten us the most effectively (in this view)

Low-calorie 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 Subjects weighed 5% more at the end, 50% more body fat

Tale of the Tape-

Low Calorie Diet

Tale of the Tape Cochrane 2002 review 0f low-fat and calorie-restricted diets: Weight

loss “so small as to be clinically insignificant.” 2001 USDA review- 28 trials of low-fat diets, 20 calorie-restricted

Average- 1700 calories per day, weight loss 9# at 6 mos, overall gain of 1# Women’s Health Initiative- 1991 NIH

49K women age 50-79, 29K usual diet, 20K low-fat diet, 8 years 20% calories from fat More veggies, fruits, whole grains 120 fewer calories per day in experimental group No less breast CA, CVD, colon CA, or stroke in experimental group 2 pounds average weight loss Waist circumference, which measures abdominal fat, increased NHLBI: “The results of this study do not change established

recommendations on disease prevention.”

Exercise 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 Hunger and intake increase in proportion to the calories expended

“Working up an appetite”

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

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 review: “Of the 34 0f 38 lower-carbohydrate diets for which weight change after diet was calculated, these lower-carbohydrate diets were found to produce greater weight loss than higher-carbohydrate diets.”

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 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

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 elevated

So 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

Inflammation

Pro-inflammatory state associated with obesity Chronic inflammation in adipose tissue- obesity stimulates macrophage infiltration,

leading to inflammatory cascade Theories- adipose tissue hypoxia; altered adipose signaling; fatty-acid activation of

innate immunity; metabolic endotoxemia Inflammation and adiposity cause insulin resistance by interfering with insulin signaling Systemic inflammatory, insulin-resistant, atherogenic state; metabolic

dyslipidemia type 2 DM and CVD Component of metabolic syndrome Associated with endothelial dysfunction All of which increases CVD risk 2012- metabolic endotoxemia- bacterial lipopolysaccaride- low-grade

inflammation Increased intestinal permeability- from high sugar diet, leads to increased plasma

endotoxin, activation of systemic inflammation Transplant of gut microbiota in mice transferred metabolic syndrome

Circ Res 2012: dietary fat lipoprotective Rodent studies- replacing refined carbs with fat (polyunsaturated, saturated,

monounsaturated) “can attenuate or prevent ventricular expansion and contractile dysfunction in response to hypertension, infarction, or genetic cardiomyopathy. … alters cardiac membrane phospholipid fatty acid composition, decreases the onset of new heart failure, and slows the progression of established heart failure. This effect is associated with decreased inflammation.”

JAMA 2004: Mediterranean diet (more whole grains, fruits, vegetables, nuts, olive oil) decreases inflammation 180 patients with metabolic syndrome over two years Experimental group lower CRP, decreased insulin resistance, improved endothelial

function Compared with “prudent diet” of 50-60% carbs, 15-20% protein, <30% fat

Inflammatory Foods Inflammation and specific foods- more research needed in general

Trans-fatty acids/partially hydrogenated oils- endothelial damage, raise LDL, lower HDL

Omega-6 fatty acids- trigger pro-inflammatory signals Nuts, seeds, vegetable oils

Sugar/refined carbs- cytokine release, increases in inflammatory PAI-1 (plasminogen activator inhibitor)

Factory-farmed animal fat- saturated fat assoc with reduced HDL anti-inflammatory activity (endothelial adhesion) Grain-fed diet high in omega-6, low in omega-3 Contains pro-inflammatory arachidonic acid- less improves rheumatoid arthritis symptoms Also Neu5Gc- body makes antibodies Processed meats (smoked, cured, salted, chemically preserved)- inflamm, colon CA

Alcohol- increases intestinal permeability, GI inflammation Dairy products- casein and lactose stimulate inflammation

Milk- lactase persistence in only 40% worldwide Monosodium glutamate (MSG)- inflammation, central obesity, type 2 DM in animals

Aspartame, many other additives Gluten- celiac disease, wheat allergy, gluten intolerance

Wheat is acid-forming and inflammatory Protective foods

Omega-3 fatty acids- fish, flaxseed, walnuts, grass-fed animals Olive oil- contains natural anti-inflammatory Antioxidants- non-citrus fruits, vegetables Spices- ginger, garlic, cinnamon, turmeric Green tea- anti-inflammatory phytochemicals

Dean Ornish

Demonstrated reversal of heart diseaseAlso- prostate CA, telomerase length,

gene expression, diabetes (decreased HbA1c and medication), BMI, lipid profile (LDL down 40%, also TG’s, total cholesterol), blood pressure, depression

Comprehensive lifestyle changesVery low-fat diet- natural, unrefined-

fruits, veggies, whole grains, legumes, soyModerate exercise- walkingStress management- yoga, breathing,

meditation, imagerySocial support- support groups, improved

relationshipshttp://www.ornishspectrum.com/proven-pro

gram/

Stress and DiabetesMore glucose and fat in the bloodStress promotes insulin resistance

Glucocorticoids make fat cells less sensitive to insulinIn order to shunt energy to muscles

Stress can encourage the immune system to attack the pancreas

Higher rates of major stressors in the three years before onset (of type I)- trigger events?

Stress increases the chances of getting DM, accelerates its development, and encourages the major complications

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 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 Sugar and refined carbs

stimulate the same dopamine pathways as addictive drugs

Grains contain exorphins Opioids like morphine or

heroin, and also addictive

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 againAlso, lower ranking humans are more likely to be obese

and more likely to be apple obese

Stress and Hierarchy Inverse relationship between health and socioeconomic

status Specific disease causes vary, but gradient remains

Synergy between stress, agriculture, and hierarchyRobert Sapolsky: “Agriculture is a fairly recent human

invention, and in many ways it was one of the great stupid moves of all time. Hunter-gatherers have thousands of wild sources of food to subsist on. Agriculture changed all that, generating an overwhelming reliance on a few dozen domesticated food sources, making you extremely vulnerable to the next famine, the next locust infestation, the next potato blight. Agriculture allowed for the stockpiling of surplus resources and thus, inevitably, the unequal stockpiling of them – stratification of society and the invention of classes. Thus, it allowed for the invention of poverty. I think that the punch line of the primate-human difference is that when humans invented poverty, they came up with a way of subjugating the low-ranking like nothing ever before seen in the primate world.”

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 (or consume other species’ dairy) As we changed our diet to first increase carbs

(agriculture), then refine them (industrialization), did we disrupt our homeostasis?

Along 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

PyramiPyramidd

PyramiPyramidd

CircleCircle

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?