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The
Nutrition Consultation in Age Management Medicine
The
leading causes of death in America are heart disease, cancer, stroke,
lung disease, injuries, diabetes, flu and pneumonia. Of these, heart
disease, cancer, stroke and diabetes are all modifiable with dietary and
lifestyle intervention. Slide
1
The goals in age
management medicine to enhance vitality, vigor and health through proper
diet, nutritional supplementation, exercise and hormone
optimization. The following slide is a curve of the average American:
age is on the X-axis; quality of life and health are on the Y-axis.
Around ages 40 to 45, quality of life and health peak out. From that
point on, they slowly decline until we die. Age management medicine is
all about rectangularizing that curve, so quality of life and health
remain optimal until just before we die. Slide
2
There are obvious
advantages to this, but a hidden advantage also exists: There will
continue to be medical breakthroughs, which can increase longevity. If
we are on the declining slope of this curve prior to entering a nursing
home, we really aren’t physically able to take advantage of these
breakthroughs—and probably wouldn’t want to. But if we can maintain
health and a high quality of life, then we would be physically able to
take advantage of these medical breakthroughs, welcoming an opportunity
to add another 10 or 15 years to our life.
Cardiovascular
Disease
Cardiovascular
disease claims more lives each year than the next 5 leading causes of
death combined, costing Americans $351.8 billion in 2003 alone.
Approximately 105 million American adults have a blood cholesterol level
equal or greater than 200 mg/dl. (1) Consider that 61.8 million
Americans have cardiovascular disease; of these, 13 million have
coronary artery disease, resulting in 2,000 deaths in the United States
daily. Also, 1 in 2.4 women die from cardiovascular disease, compared to
1 in 29 from breast cancer. If we could eliminate all major forms of
cardiovascular disease, we could add 7 years to our life expectancy.
Slide 3
Clearly, as Galen said, “Prevention is better than cure.”
Healthy
Endothelium: The primary role of the endothelium is to maintain vascular
tone, accomplished by different dilators and constrictors. The major
vasodilators that are endothelium-derived include nitric oxide and
Prostacylin (PC). Prostacylin works synergistically with nitric oxide
to inhibit platelet aggravation. Bradykinin stimulates nitric oxide and
Prostacylin and endothelium-derived hyperpolarizing factor. It also
stimulates tissue plasminogen activator (fibrinolysis).
The most potent
endothelium-derived vasoconstrictor is endothelin. Angiotensin II
stimulates the production of endothelin, and it is a pro-oxidant. Both
angiotensin II and endothelin promote smooth muscle cell proliferation
and contribute to plaque formation.
Functions of
nitric oxide: Nitric oxide mediates endothelium-dependent vasodilation.
It inhibits platelet adherence and aggregation as well as inhibits
proliferation of smooth muscle cells. It prevents oxidative
modification of LDL cholesterol. When nitric oxide production is
impaired, it promotes atherosclerosis. Vasoconstriction, platelet
aggregation, smooth muscle cell proliferation and migration, leukocyte
adhesion and oxidative stress are all accelerated as nitric oxide levels
are diminished.
Slide 4 Therefore, the
mechanisms for reducing endothelial and nitric oxide availability and
increasing endothelial dysfunction are all promoted by
hypercholesterolemia, hypertension, diabetes and smoking. These all
produce reactive oxygen species, which in turn inhibit the production of
the enzyme DDAH, resulting in increased levels of nitric oxide synthase
inhibitor—resulting in decreased endothelial nitric oxide availability.
(2)(3)
Reactive oxygen
species also reacts with nitric oxide, causing a loss of nitric acid
bioactivity. Reactive oxygen species also cause oxidative degradation of
H4B, which is a critical nitric oxide synthase cofactor. That results in
decreased endothelial nitric oxide availability, which increases
endothelial dysfunction.
The oxidation of LDL in
the vessel wall hastens the atherogenic process by recruiting
macrophages, stimulating auto antibodies, increasing LDL uptake and
increasing vascular tone and coagulability. Supplementation with
antioxidants may act to inhibit this oxidation, retarding, or even
preventing, the formation of atherosclerotic plaque. (4)
Lipids &
Cardiovascular Disease
LDL cholesterol is a
major cholesterol carrier in the blood. LDL cholesterol promotes
atherosclerosis and is influenced by genetics, high-saturated fatty acid
diets and inactivity. Secondary causes include diabetes,
hypothyroidism, obstructive liver disease, chronic renal failure and
certain drugs.
HDL cholesterol
carries cholesterol away from the arteries. HDL cholesterol removes
excess cholesterol from atherosclerotic plaque and has antioxidant and
anti-inflammatory properties. It is influenced by genetics, insulin
resistance, high triglyceride levels, overweight and obesity,
inactivity, cigarette smoking, high-carbohydrate diets and certain drugs
like beta-blockers, anabolic steroids and progestational agents.
Triglycerides are
obtained from the blood and also made by the liver. They are
transported through the blood on either chylomicrons or VLDL.
Triglycerides are influenced by genetics, obesity, insulin resistance,
inactivity, smoking, high-carbohydrate diets and diseases, such as Type
2 diabetes, chronic renal failure and nephrotic syndrome, excess alcohol
and certain drugs, including corticosteroids, oral estrogen and
retinoids.
LDL cholesterol
is the primary atherogenic factor. Trial after trial has shown that
lowering LDL drives down cardiac events. Low HDL remains an important
independent risk factor for cardiac events. The Air Force/Texas
Coronary Atherosclerosis Prevention Study (5) (6) showed that
aggressive statin therapy is an appropriate treatment for low HDL
syndrome. Triglycerides are a secondary risk factor in coronary artery
disease.
The “Big Four”
low-LDL trials are . . .
-
Heart Protection Trial from Great
Britain, published in Lancet in 2002 (7)
-
Pravastatin or Atorvastatin Evaluation
and Infection Therapy-Thrombolysis in MI 22 (PROVE –IT) Trial. The
PROVE-IT trial was published in the New England Journal of
Medicine in 2004. (8)
-
“A to Z” Trial. The “A to Z” Trial was
published in JAMA in 2004. (9)
-
Treating to New Targets, published in
the New England Journal of Medicine 2005. (10)
Slide 5
The bottom line
to all these trials is that LDL should be lowered to less than 70 in all
patients with recent or remote coronary artery disease. Ultra-low LDL
should also be a goal for all diabetic patients and patients with
metabolic syndrome.
Can a low
cholesterol/saturated fat diet help reduce LDL? The truth is that diet
has minimal effect on reducing LDL. Statins must be used as the primary
therapy for LDL management with diet as a supplementary factor.
Non-Pharmacologic Ways To Decrease
Cholesterol
-
Reduce saturated fat and completely
avoid trans-fat in the diet.
-
Increase fiber: 25-35 grams of fiber
are recommended per day. Good sources of soluble fiber include
beans, lentils, apples, citrus fruits, oats, oat bran, apple pectin,
barley, peas, carrots and freshly ground flaxseeds. Eating 5 grams
of soluble fiber daily has been shown to decrease LDL by 5%.
-
Increase Omega 3s. A handful of almonds
(70 grams) daily can decrease LDL by 8%. You can also get
molecularly distilled fish oil.
-
Substitute and increase soy protein in
place of animal protein. One study showed 13% drop in LDL when
eating 50% soy, compared to 8% on meat protein only.
-
Green tea (240 mg to 320 mg of
polyphenols) has been associated with lower LDL-cholesterol and
lower risk of death from coronary artery disease. Daily
recommendation: 4 to5 cups.
Supplements Shown To Decrease Cholesterol
-
Gugulipid: A resin, used in Ayurvedic
medicine. In studies, guggul has lowered total cholesterol by more
than 20% while increasing HDL by 36% without dietary adjustments.
The active constituent is guggalsterone—which acts to halt bile acid
production—leading to a reduction of cholesterol and
triglycerides. Dose of 1500 mg, 3 times a day is recommended; the
max dose is 6 grams a day.
-
Red yeast rice (Cholestin in other
countries): Contains seven different statins, derived from strains
of red yeast, cultivated on rice used for centuries in China. Be
sure to check the label to verify the product contains a red rice
yeast extract. The brand “Cholestin” by Pharminex was the only one
verified in studies to significantly decrease cholesterol, but this
was banned from the United States for containing the same compound
as Lovastatin.
-
Arjuna Bark: Used in Ayurvedic medicine
and a strong antioxidant. Capsule form. Dose is 1-3 grams per day.
-
Prickly Pear Extract: A small Italian
study in 2003, published in the Nuclear Medicine Review of
Central and Eastern Europe, indicated prickly pear extract can
lower LDL cholesterol. (11) The supplements used in the study had no
affect on levels of HDL or triglycerides.
-
Ultrameal: A combination product with
soy, fiber and plant sterols, shown to reduce LDL by 33% along with
a Mediterranean diet.
Anyone taking
statins definitely needs to supplement with coenzyme Q10. Statin drugs
deplete the body of coenzyme Q10, an essential supplement for providing
energy to the body’s cells, especially heart and muscle cells needing
more energy. Coenzyme Q10 depletion can result in muscle damage also
associated with aches and pains. Since the heart is basically a muscle,
it may be damaged as well, which would obviously impair its ability to
pump blood and increase the risk of congestive heart failure. Over time
statins can weaken the heart and impair its function. Coenzyme Q10 is a
powerful antioxidant, shown to be beneficial for heart health by
preventing the oxidation of LDL cholesterol and supporting energy
metabolism at the cellular level.
Plant sterols,
stanols and LDL. The value of
sterols and stanols really center around the structural similarities
between cholesterol and phytosterols. Phytosterols can displace
cholesterol from micells in the process of cholesterol absorption from
the gut. This displacement of cholesterol from the micelle decreases
cholesterol absorption from the gut by 30% to 50 %. (12)(13) This can
significantly decrease serum cholesterol levels in those who regularly
consume phytosterols. The addition of 2 grams of sterol ester to a
standard Western diet results in a 10% decrease in LDL cholesterol
levels without a significant effect on HDL or triglyceride levels. (14)
The U.S. National Cholesterol Education Program (NCEP) recommends a
dietary phytosterol intake of 2 gm/day. (15) This results in a 10%
reduction in LDL cholesterol, inferring a 25% decrease in cardiovascular
disease (16). Finally, there seems to be an additive effect with the
combination of phytosterols and statins in the LDL-cholesterol-lowering
objectives. (17)
Hyperhomocysteinemia and cardiovascular disease.
Homocysteine is a substance produced when the body breaks down the amino
acid methionine. High levels of homocysteine are inflammatory and
injure arterial endothelial cells, which promotes proliferation of
arterial smooth muscle cells, vascular inflammation, atherogenesis and
destabilization of established plaque. (18) Deficiencies of folic acid,
vitamin B6 and B12 are associated with hyperhomocysteinemia. Whether
correction of elevated homocysteine levels with vitamins reduces
vascular events is currently under investigation. (19) In 1999, the
American Heart Association recommended all patients with a family
history of cardiovascular disease should exceed the recommended dietary
allowance values for folic acid, vitamin B6 and vitamin B12. (20)
Treating
hyperhomocysteinemia: At this time, there is no consensus on
homocysteine management, regarding B vitamin supplementation. Baseline
serum levels of B12 should be checked prior to supplementation to avoid
masking a B12 deficiency. Dosages of B6 greater than 500mg/day are not
recommended and may cause irreversible nerve damage. (21)
A Side Note
About Homocysteine Levels & Sample Handling
Homocystine is
released from cells in whole blood left at room temperature. Rapid
separation of plasma homocysteine is required for test reliability. The
plasma should be cooled on ice immediately, then frozen below -20 °C
until time of analysis. (22)
Nutrition &
Inflammation
Slide 6
Nutrition, it
turns out, is a key player in preventing or causing low-grade cellular
inflammation. This manifests in the form of weight gain, high glycemic
diets, trans-fats, obesity, saturated fats, low monounsaturated fatty
acids, low-fiber diet, metabolic syndrome, low omega-3 diets,
hyperglycemia and glycation, and high polyunsaturated fatty acid diets.
Inflammation &
Dental Health
Periodontal
disease may increase the risk of cardiovascular disease by approximately
20%, so the dentist plays a key role in helping control and prevent
cardiovascular disease. Other contributors to inflammation in the
dental world would be aggressive teeth brushing, aggressive flossing and
plaque. The recently marketed counter-rotational and
oscillating-rotating electric brushes have shown to reduce levels of
gingival bleeding and inflammation.
Visceral
Adiposity
The most critical
factor in reducing inflammation is loss of adiposity, especially
visceral adiposity. We used to think adipose tissue was just dormant—now
we know it’s anything but dormant. It is quite metabolically active,
producing Interleukin-6, which causes increased C-reactive protein
levels. IL-6 is a powerful pro-inflammatory cytokine and is the most
important factor in controlling hepatic acute-phase response (hs-CRP).
Total body adiposity is the single most important determinant of serum
IL-6 concentrations. (23)(24) Adipose tissue also produces Tumor
Necrosis Factor Alpha and causes insulin resistance.
Slide 7
The obesity
problem in America. Today two-thirds of Americans are overweight or
obese. Almost one-third of all Americans are obese. The prevalence of
overweight people has increased 50% in all populations since 1960. One
in four children are overweight. Americans have decreased fat intake
from 42% to 34% of total calories since 1960. In spite of that, American
children may have a shorter like expectancy than their parents because
of obesity-related illnesses. The number one cause of liver disease in
America is fatty liver.
How do we assess
overweight and obesity?
Slide 8
The body
mass index is the weight in pounds, divided by height (in inches) and
squared x 703. However, the body mass index does not accurately reflect
how much body fat an individual has. Estimates of total body fat include
skin-fold measurements, bioelectrical impedance, total body conductivity
methods, hydrostatic weighing and DEXA scan. Body fat distribution is
another way to assess overweight and obesity, which can be done by waist
measurement, an inch above the umbilicus. The waist-to-hip ratio also is
used, though it isn’t as accurate as waist circumference. The greatest
risk for men is a waist-to-hip ratio greater than 1; for women, it is
greater than 0.8. (26)(27).
Slide 9
This brings us to
the metabolic syndrome, which is a huge cause of inflammation.
Metabolic
Syndrome
Metabolic
syndrome—also known as Syndrome X or Insulin Resistance Syndrome—is a
cluster of metabolic risk factors for coronary heart disease and
cognitive decline. Features of this syndrome include abdominal obesity,
insulin resistance, dyslipidemia, hypertension and elevated levels of
cytokines and adhesion molecules . . . in other words, increased
inflammation.
Slide 10
The risk factors
for metabolic syndrome include men whose waist is greater than 40 inches
(measured an inch above the umbilicus) and women with waists greater
than 35 inches; triglycerides of 150 or greater; HDL-cholesterol (men
less than 40, women less than 50); blood pressure equal to or greater
than 130/85; and a fasting blood sugar of 100 or greater. Having any
three of these meets the criteria for metabolic syndrome. (28)(29)
Slide 11
Visceral fat –
central fat or abdominal fat are all associated with the greatest
metabolic risk. Metabolic syndrome is present in 23.7% of U.S. adults.
And 43.5% of individuals 60 years and older have metabolic syndrome; 30%
of obese children have metabolic syndrome. The end result is we now
have almost 50 million Americans with metabolic syndrome.
The consequences
of metabolic syndrome are horrendous. Individuals with metabolic
syndrome experience a six-fold higher rate of cardiovascular events and
mortality than the general population.
Published in
1998: Soon metabolic syndrome will overtake cigarette smoking as the
number one risk factor for heart disease among the U.S. population. Now,
metabolic syndrome has overtaken cigarette smoking as the number one
risk factor for heart disease in the United States. (30)
Mechanisms
involved in the production of obesity-related low-grade inflammation.
Fat tissue is an important source
of pro-inflammatory Tumor Necrosis Factor Alpha and Interleukin-6, and
anti-inflammation (adiponectin) cytokines. Elevated pro-inflammatory
cytokines can lead to insulin resistance by interfering with the
anti-inflammatory effects of insulin.
Obesity
is characterized by oxidative stress; excessive oxidative stress leads
to increased production of Reactive oxygen species. Dietary restriction
leads to reduction in oxidative stress and inflammation.
Insulin
resistance is the key factor in metabolic syndrome, making it so
deadly. Insulin resistance is central to the metabolic syndrome and to
Type 2 diabetes. Insulin resistance perpetuates the diabetic state and
is directly related to adiposity. Omental fat in the intramyocellular
compartment plays the key role. An increased ratio of trunk to leg fat
is more highly correlated with insulin resistance than is BMI.
Type 2
Diabetes
In the U.S., 17
million people have Type 2 diabetes. Sadly, 5.2 million of them remain
undiagnosed—equating to almost a third of all diabetics in this
country. If we look at age-adjusted prevalence in people age 20 years
or older by race and ethnicity, we find 17.6% of the American Indians
and Alaska Natives population are Type 2 diabetic. Additional stats:
non-Hispanic blacks, 12.5%; Hispanic and Latino Americans, 11.4%;
non-Hispanic whites, 7.7%.
By 2025 (less
than 20 years from now), the prevalence is estimated to increase to
nearly 22 million or roughly 9% of our population. This is not only a
problem in our country, but also worldwide. In 2000, there were 171
million Type 2 diabetics in the world; by 2030, there will be 366
million worldwide.
What are the risk
factors for Type 2 diabetes? The first one is age (45 years old or
older), being overweight (BMI of 25 or greater), having metabolic
syndrome, a family history of diabetes, habitual physical inactivity,
race and ethnicity, previously identified abnormal fasting blood sugar
of 100 or greater or an abnormal glucose tolerance test, a history of
gestational diabetes or delivering a baby weighing 9 pounds or more,
hypertension 140/90 or higher, an HDL of less than 35 and/or a
triglycerides of 250 or greater, polycystic ovary syndrome and a history
of vascular disease.
We used to call
Type 2 diabetes adult-onset, but we can no longer do that because we now
have an epidemic of Type 2 diabetes in children and adolescents in this
country. The youngest Type 2 diabetic in the U.S. is 4 years old. Type
2 diabetes severely impacts the health of our society. Type 2 diabetics
have a 5 to 10 year reduction in their life expectancy—and CVA and MI
are increased by 5. Approximately 75% of type 2 diabetics will die of
coronary artery disease.
The natural
history of Type 2 diabetes starts with adiposity.
Slide 12 Adiposity results in
insulin resistance, which is the primary defect, then after that the
beta cells of the pancreas compensate by increasing insulin production.
This ultimately results in beta cell exhaustion, which is the secondary
defect. Next is pre-diabetes, followed by full-blown Type 2 diabetes and
then, insulin-requiring Type 2 diabetes since the beta cells become
completely burned out. This is the absolute insulin deficiency state.
Targeting
Inflammation & Insulin Resistance
The
Thiazolidinediones (TZD) act directly to reduce insulin resistance. They
also appear to improve beta cell function and have anti-inflammatory
properties. TZDs have become quite popular in the treatment of Type 2
diabetes and reduce C-reactive protein and MMP-9 (stabilize plaque from
rupture). TZDs also suppress two key acute-phase proteins-CRP and serum
amyloid A. Finally, TZDs suppress production of pro-inflammatory
cytokines.
Metformin is used
frequently in this country to treat Type 2 diabetes. The home study
entitled “Hyperinsulinemia: The outcome of its metabolic effect” reviews
all this. Treatment with metformin for 16 weeks showed a significant
improvement in endothelial function, but not in chronic, low-grade
inflammation. Metformin decreases plasma levels of VCAM-1, E-selectin,
t-PA, PAI-1. C-reactive protein levels were not affected. (31)
As little as a 5%
weight loss can significantly reduce fasting blood sugars and insulin
levels as well as reduce inflammatory markers. When lifestyle
intervention produces a weight loss of 5% to 7%, there is a 58%
reduction in the number of cases of Type 2 diabetes over a 4-year
period.
Orlistat:
Treatment For Obesity
Used for
long-term management of obesity, orlistat is a lipase inhibitor with a
recommended dose of 120mg t.i.d., 20 minutes prior to each meal. It has
pharmacological lipid-lowering effects, improves insulin resistance and
decreases body fat and serum leptin levels. Orlistat combined with diet
and exercise significantly reduces BMI, waist circumference, HOMA IR,
hs-CRP, leptin and increased adiponectin. It significantly reduces risk
for diabetes. It also reduces markers of chronic inflammation, so it is
anti-atherogenic.
In summary,
decreasing body fat results in a decreased LDL, decreased triglycerides,
improved insulin sensitivity, reduced total cholesterol, improved HDL
and decreased inflammation. Slide
13
How do we get rid
of body fat? Firstly, by keeping insulin and glucose levels as low as
possible. That is absolutely essential. With elevated insulin levels,
people cannot burn body fat for energy. It is physiologically
impossible. Exercise (both aerobically and anaerobically) increases
metabolic rate and actually can turn people into an energized
“fat-burning machine!” Resistance training preserves muscle mass while
losing body fat. The more muscle mass people have the more calories
they burn at rest. The more aerobically fit people are the more
efficient they are at burning body fat for energy.
Dietary Fiber
& Inflammation
The NHANES study
with 4,900 adults, whose median CRP level was 2.0, showed subjects who
ate the most fiber had the lowest CRP levels. CRP was inversely related
to the amount of fiber people ate. Also, the more fiber people ate, the
more weight they lost. Weight loss equal to or greater than 10% has
been associated with the greatest reduction of inflammatory markers of
inflammation. (32)
A closer look at
fiber content in foods: Many fruits are quite high in fiber, as are
vegetables and grains. Legumes (such as green peas, kidney beans, pinto
beans and lentils) all have high fiber content, as do nuts and seeds.
High-fiber cereals are another easy way to increase fiber
intake—although they are a processed food and should be used in
moderation to other natural foods.
Slide 14
Slide 15
Slide 16
Fats & Inflammation
Classification of fatty acids. Slide17
Saturated fats have no double bonds and are
solid at room temperature. The major source of saturated fats comes
from animals, including meat and dairy products. Other sources include
palm oil and coconut oil. Saturated fats should not exceed 10% of our
total caloric intake. Red meat should be limited to once or twice a
month. Saturated fats contribute significantly to the inflammatory
state.
Unsaturated fats
have one or more double bonds and are liquid at room temperature. The
unsaturated fats include monounsaturated fatty acids, such as olive oil,
canola oil, avocados and nuts.
The
polyunsaturated fatty acids fall into three categories:
-
Omega-3 fatty acids, such as fish oil,
flaxseed, walnuts and soybeans. They are anti-thrombotic and
anti-inflammatory.
Slide18
-
Omega-6 fatty acids, present in most
seeds, vegetable oils (such as corn oil, safflower oil and sunflower
oil) and meats. They are pro-thrombotic and pro-inflammatory .
-
Trans-fats are man-made as well as
highly inflammatory and atherogenic. They are formed by the
industrial hydrogenation of vegetable oils (i.e. man-made fat).
Average consumption in the U.S. is 4% to 7% of total fat calories.
Data supports an association between TFA intake and systemic
inflammation. Some experts consider TFAs to be the major cause of
CAD. The impact of TFAs on human lifespan and degenerative disease
is unknown at this time; we will find out in 20 to 30 years.
Mensink and Katan in 1990 looked at the effect of trans and
saturated fat (10% calories) on blood lipids versus monounsaturated
fat. (36) The results are shown in
Slide19
Hu, et al in 1997
compared the various fatty acids and their effect on CHD. See Slide20
for the astounding results of this study. (37)
Levels of trans-fats must be on food
labels. Dietary sources rich in trans-fats include store-bought
cookies, crackers, baked goods, margarine and commercial deep-frying
oils as well as the foods cooked in them. Labels may claim to contain “0
grams trans fat,” if they have less than
0.5g per serving. Read labels for partially hydrogenated oil.
If they’re present, avoid them!
Slide21
Monounsaturated fats are the omega-9 fatty
acid group. Monounsaturated fatty acids reduce inflammation. Most of
our dietary fat should come from monounsaturated fatty acids or the
omega-9s. Olive oil should be the predominant oil consumed to assure a
diet high in monounsaturated fatty acids and low in saturated fat.
Olive oil (extra virgin) is the preferred most healthy form of olive
oil. Canola oil contains healthy omega-9 fats as well as
pro-inflammatory omega-6 fats and should be used sparingly. Peanut oil,
like canola oil, also contains pro-inflammatory omeg-6 fats and a fair
amount of saturated fats—and should be used sparingly. Avocados and
almonds, cashews, macadamia nuts, pecans and pistachios are all great
sources of omega-9 monounsaturated fatty acids.
Omega-6/Omega-3 ratios: Americans consume
large amounts of vegetable oils, which are quite high in omega-6s, such
as corn oil, safflower oil, sunflower oil and cottonseed oil. Americans
also eat large quantities of meats, obtained from domesticated animals
that have been fed grains high in omega-6 fatty acids. Americans also
take in very little omega-3 fatty acids. The end result is an omega-6
to omega-3 fatty acids ratio of about 14:1 to 20:1. In the early human
diet, it was 1:1. Should this ratio be greater than 10:1, we are put at
high risk for inflammation and thrombosis.(33)(34)
Slide22
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