I only use one study to show me what I should be eating. Eat like a 1950's Okinawan. They often live to 100 and still have their mind and body working.
Back in the 1950's the Japanese rural Okinawan group of people had
the most centenarians per capita. How did they live so long? Here is
their diet
Caloric Restriction, the Traditional
Okinawan Diet, and Healthy Aging
The Diet of the World’s Longest-Lived People and Its Potential Impact on Morbidity and Life Span
Ann. N.Y. Acad. Sci. 1114: 434–455 (2007).
TABLE 1. Traditional dietary intake of Okinawans and other Japanese circa 1950
Total calories 1785
Total weight (grams) 1262
Caloric density (calories/gram) 1.4
Total protein in grams (% total calories) 39 (9)
Total carbohydrate in grams (% total calories) 382 (85)
Total fat in grams (% total calories) 12 (6)
Saturated fatty acid 3.7
Monounsaturated fatty acid 3.6
Polyunsaturated fatty acid 4.8
Total fiber (grams) 23
Food group Weight in grams (% total calories)
Grains
Rice 154 (12)
Wheat, barley, and other grains 38 (7)
Nuts, seeds Less than 1 (less than 1)
Sugars 3 (less than 1)
Oils 3 (2)
Legumes (e.g., soy and other beans) 71 (6)
Fish 15 (1)
Meat (including poultry) 3 (less than 1)
Eggs 1 (less than 1)
Dairy less than 1 (less than 1)
Vegetables
Sweet potatoes 849 (69)
Other potatoes 2 (less than1)
Other vegetables 114 (3)
Fruit less than 1 (less than 1)
Seaweed 1 (less than 1)
Pickled vegetables 0 (0)
Foods: flavors & alcohol 7 (less than 1)
Data derived from analysis of U.S. National Archives, archived food records, 1949 and based on survey of 2279 persons.
Some points
Their diet was 85% carb, and 6% fat. Sweet potatoes (a Japanese sweet potato) made up almost 70% of their calories. Nuts were less than 1% of calories (the equivalent of 1/10 of an ounce a day) Oil was less than 2% of calories (which is about 1 tsp a day) and sugars were less than 1% of calories (less than a tsp a day)
The total animal products including fish was less than 4% of calories which is less then 70 calories a day. That is the equivalent of around 2 oz of animal products or less a day.
This is a population group worth idolizing, not a short lived population of eskimos or blood and raw milk drinking African tribes who live till the age of 40.
Looking at dairy:
The consumption of dairy in children has resulted in earlier puberty. "The effect of animal protein intake, which was associated with an earlier puberty onset, might mainly be due to dairy. "An earlier puberty onset has been related to an increased risk for hormone-related cancers in adulthood. For example, a meta-analysis of 26 epidemiological studies reported a9% risk reduction for breast cancer with every additional year at menarche. Additionally, recent study results demonstrated that a 1-y delay in menarche was associated with a 2.4 to 4.5% lower total mortality.
http://jn.nutrition.org/conten...
The concern with dairy and hormone dependent cancer is something to think about as well. It has been shown that consuming dairy significantly increases circulating steroid hormones in woman and that vegetarians have far less of this hormone. "In conclusion, greater consumption of red meat and dairy products might influence circulating concentrations of SHBG and estradiol, respectively. Given the well-established role of steroid hormones in breast cancer etiology for postmenopausal women, these findings may have important health implications" Tumor growth from these hormone imbalances is also evident "A dramatic increase in estrogen-dependent malignant diseases, such as ovarian, corpus uteri, breast, testicular and prostate cancers has been recognized. Ganmaa et al. investigated the incidence and mortality of testicular and prostate cancers in relation to dietary practices. Among various food items, cow’s milk and cheese had the highest correlation with incidence and mortality rate of these cancers" Children are at high risk "Among the exposure of humans, especially prepubertal children, to exogenous estrogens, we are particularly concerned with" These xenoestrogens from lactating preganant cattle (the majority of commercial cattle used for milk) significantly raised estrogen levels in male adults and reduced testosterone levels and did even more so in children. This is significant since these estrogens have mutagenic affects "Toxicological and epidemiological studies have indicated that E2 could be categorized as a carcinogen. Milk is considered to be a rich source of estrogens." Indeed, E2 concentration is higher in mammary drainage than in the peripheral circulation in high yielding cows."
http://missclasses.com/mp3s/Pr...
http://missclasses.com/mp3s/Pr...
http://birdflubook.com/resourc...
Again, these harms are independent of organic, grassfed, conventional, or raw. Xenoestrogens are inherent of dairy.
Regarding animal products which includes fish, eggs, meat, poultry and dariy:
Cancer is said to be a disease of old age, that is because we are living longer, we are encountering more carcinogens which further mutate our DNA which can lead to uncontrolled cell growth. This biological hypothesis goes against what is actually observed "Accordingly, it has been reported that the mortality due to cancer constantly decreases after the age of 85–90 years [3]. Therefore, it seems that centenarians are endowed with a peculiar resistance to cancer."
Why do centenarians escape or postpone cancer?
The role of IGF-1, inXammation and p53
http://www.google.com/url?sa=t...
Cell growth is determined primarily by the growth hormone Insulin like growth factor, also called IGF-1. As a child, this growth hormone is found in much larger amounts and then slowly tapers off during adulthood. Increased levels of circulating IGF-1 as adults can promote unwanted growth, particularly in the form of tumors. An association can be seen in the following meta-analysis between increased IGF-1 levels and prostate cancer. "Our meta-analysis revealed that the body of the world-wide published literature is consistent with an average 21% increased risk of prostate cancer per standard deviation increase in IGF-I"
http://www.ncbi.nlm.nih.gov/pm...
A similar association is revealed between increased IGF-1 levels and breast cancer "The results of this collaborative analysis show that plasma concentrations of IGF1 are positively associated with breast-cancer risk."
http://www.ncbi.nlm.nih.gov/pm...
Elevated IGF-1 has also been shown to increase the chance of the cancer to metastasis. This hormone is responsible for cancer proliferation, survival, migration and angiogenesis (feeding cancer with blood supply)
http://edrv.endojournals.org/c...
IGF-1 deficiency leads to dwarfism and one might expect this group of the population to not get cancer, as is the case. "The individuals with GHR
deficiency (GHRD) exhibited only one non-lethal malignancy and no cases of diabetes, in contrast to 17% cancer and 5% diabetes prevalence in
the controls."
http://www.ncbi.nlm.nih.gov/pm...
A fascinating study involved studying cell line apoptosis, that is, cancer cell death. "Fasting serum was obtained from postmenopausal women
participants at the Pritkin Longevity Center Residential Program where they were placed on a low-fat (10-15% Kcal), high-fiber (less than 40
gm/d) diet and attended daily exercise classes for 2 weeks." They used the blood of this group and dripped it on cancer cell lines. Significant cell death was observed as well as reduced IGF-1 levels in the blood. This can be seen here in the study below.
http://www.pritikin.com/epersp...
In an attempt to "determine the underlying mechanisms for these anticancer effects", cell apoptosis was again to be examined when the blood of a group eating a similar diet was dripped on a cancer cell line. What made this study so remarkable, was that not only did cancer cells die off in greater abundance when IGF-1 levels were lowered through diet, but that the cell death benefits were nulled when the researchers put back the IGF-1 into the blood and re dripped it on the cell line. It was also discovered that IGFBP-1, the protein that binds up the IGF-1 hormone, was found in greater quantities on a low fat, high fiber diet.
http://www.ncbi.nlm.nih.gov/pm...
"The aim of this cross-sectional study was to determine whether a plant-based (vegan) diet is associated with a lower circulating level of insulin-like growth factor I (IGF-I) compared with a meat-eating or lacto-ovo-vegetarian diet among 292 British women, ages 20 –70 years" It was found that vegetarians and omnivores had very similar numbers in terms of IGF-1 levels, and one truly has to eliminate all animal products to have optimal levels of IGF-1 and IGFPB-1.
http://www.ncbi.nlm.nih.gov/pm...
"These considerations enable the prediction that a low-fat vegan diet will be profoundly protective with respect to risk for postmenopausal breast
cancer. The protein content of this diet will preferentially support glucagon activity and possibly decrease IGF-I synthesis." As I will discuss, it is indeed the protein "quality" of the food that determines IGF-1 overproduction.
http://img2.timg.co.il/forums/...
The protein content of our food triggers IGF-1 production from the liver. "Amino acid availability to the hepatocytes is essential for IGF-I gene expression". Therefore, excess protein can result in excess IGf-1 levels.
http://www.ncbi.nlm.nih.gov/pu...
This raises the question seen with other studies though. "Previous data on the associations between dietary intake and IGF-I levels are sparse. Consistent with our data, other cross-sectional studies have also found no association between total protein intake and serum age-adjusted IGF-I levels in men (17, 18) or women (16). However, these studies have not investigated the effects of different types of protein intake on serum IGF-I and its main binding proteins." The key phrase here is that different types of protein have different effects on our liver.
IGF-1 increased with animal protein intake and decreased with plant protein intake. The inverse is true for IGFBP-1 (the binding protein). "In
summary, these results suggest that total IGF-I concentration is lower among women who adopt a vegan diet. In addition, IGFBP-1 and IGFBP-2
concentrations are substantially higher in vegan women compared with meat-eaters and vegetarians, suggesting that the amount of bioavailable IGF-I may be lower in vegan women. The nutritional characteristics of the vegan diet that account for these differences are not clear but may be related to vegans’ lower intake of protein high in essential amino acids. These results suggest that even when total
protein intake is not notably low, a low intake of essential amino acids, as typically found in a plant-based diet, may be sufficient to reduce serum IGF-I and increase serum IGFBP-1 and IGFBP-2 levels."
http://cebp.aacrjournals.org/c...
To summarize this biological phenomenon, when a food source is consumed that has similar protein structure and amino acid proportions to our own
body, our liver reacts by releasing IGF-1 as well as storing IGFBP-1. "Another mechanism through which a vegan diet may influence IGFBP-1 levels is via an enhanced insulin sensitivity. A diet low in saturated fat and high in dietary fiber and complex carbohydrates may reduce insulin secretion, both directly by reducing the postprandial glycaemic response (39, 40), and indirectly by reducing adiposity (41), causing a large increase in the production of IGFBP-1 within the liver (42)."
Looking at inflammation:
There is another aspect to developing a chronic
illness such as cancer, that has yet to be disscussed. Chronic low grade inflammation has been implicated in the development of chronic illnesses and diet is the primary cause of this inflammation. "Inflammation is a pathological condition underlying a number of diseases including cardiovascular diseases, cancer, and chronic inflammatory diseases. In addition, healthy, obese subjects also express markers of inflammation in their blood. Diet provides a variety
of nutrients as well as non-nutritive bioactive constituents which modulate immunomodulatory and inflammatory processes. Epidemiological
data suggest that dietary patterns strongly affect inflammatory processes." Phytonutrients found in plants can regulate inflammatory markers in humans as explained in great detail here.
http://193.146.160.29/gtb/sod/usu/$UB...00435_Watzl.pdf
The effect of a single high fat meal has been known to impair endothelial function in ones artieries, possibly causing ones risk of LDL cholesterol to oxidize to increase significantly. "The high-fat meal (900 calories, 50 g of fat, 14 g of saturated fat, and 255 mg of cholesterol) consisted of an Egg McMuffin®, Sausage McMuffin®, 2 hash brown patties, and a noncaffeinated beverage (McDonald's Corporation). The isocaloric low-fat meal (0 g of fat, 13 mg of cholesterol) consisted of Frosted Flakes® (Kellogg Company, Battle Creek, Michigan), skimmed milk, and orange juice. Lipoprotein and glucose determinations were
repeated 2 and 4 hours after eating." The effect of inflammation can be seen below, and lasts for several hours following ingestion. This amount of fat is not that uncommon for a meal in the current American diet, and constant consumption of eating these high fat foods results in chronic inflammation.
http://www.sciencedirect.com/s...
This inflammation can also be seen to occur in our lungs after a high fat meal. "These results demonstrate that a HFM, which leads to significant increases in total cholesterol, and especially triglycerides, increases exhaled NO. This suggests that a high-fat diet may contribute to chronic inflammatory diseases of the airway and lung." The data table showing the inflammation can be seen below.
Why is it that our body reacts in this way after a meal high in fat? It is an immune response to a percieved threat. It has been hypothesized
that it is the animal protein itself that causes the body to become inflamed as theorized with Rheumatoid Arthritis in this case report of a women who ceased animal protein intake and recovered from her RA outbreaks.
http://ncp.sagepub.com/content...
Whipped cream caused a similar effect in inflammation. It was discovered that pre and post meal, endotoxins were found in the blood stream. Endotoxins are bacterial toxins that can trigger our immune system to become inflamed.
The question now is where are the endotoxins coming from. It was hypothesized that the bacteria from the gut was causing the endotoxemia. The saturated fat found in these animal products were acting as a pathway for the endotoxins to enter our blood stream. "Because the human gut is host to 100 trillion commensal organisms, which together contribute to an enteric reservoir of 1 g LPS (8), we hypothesized that most of the circulating endotoxin may derive from the gut and that a small amount of commensally derived ] LPS maycotransit with dietary fat from the gut after a high-fat meal, which thereby increases plasma endotoxin concentrations postprandially"
This idea that saturated fat acts as a pathway out of our intestines is known as a leaky gut, as in the permeability of our intestines is increased after a high fat meal. "saturated fats also appear to increase the permeability of intestinal epithelium and contribute to the breakdown of the intestinal barrier."
http://www.ncbi.nlm.nih.gov/pm...
http://ajcn.nutrition.org/cont...
As seen in this study, "Subjects from the first group...were asked to ingest a 910-calorie HFHC meal (egg muffin and sausage muffin sandwiches and two hash browns, which contain 88 g carbohydrates, 51 g fat [33% saturated] and 34 g protein [carbohydrates 41%, protein 17%, and fat 42%]), while subjects from the second group (six males, BMI 22.8 0.6 kg/m2, mean age 31.2 1.1 years) were given an isocaloric meal rich in fruit and fiber consisting of oatmeal, milk, orange juice, raisins, peanut butter, and English muffin (carbohydrates 58%, protein 15%, and fat 27%)"
After the high fat meal, endotoxin level significantly increased
We now run into a problem. Looking at this chart, we see that the timescale is only 3 hours. If the hypothesis that our own gut flora is causing the inflammation is correct, then we should see the spike in inflammation several hours later, as the large intestine is where the bacteria lie. A new hypothesis must come from this, as our own gut flora cannot be causing this inflammation. One might hypothesize that the endotoxins are coming from the food itself, and this is what we indeed
find. "We therefore aimed to determine whether common foodstuffs may contain appreciable quantities of endotoxin or other similar agents that
may be capable of eliciting innate immune activation of human monocytes....Forty extracts were therefore prepared from twenty-seven
foodstuffs common to the Western diet, and the capacity of each to induce the secretion of IL-6 and TNF-α from human monocytes was measured
and compared " The capacity of these foods to cause white blood cells to secrete inflammatory signals was measured.
"These findings therefore suggest that apparently unspoiled foodstuffs may nevertheless contain at some point in their preparation or processing a
sufficient microbial load to release TLR2 and TLR4 stimulants into their growth environment. This notion is supported by many previous
studies showing that certain commonly consumed foodstuffs can contain a high bacterial load before cooking, such as fresh beef mince which has often been shown to contain approximately 105–107 colony forming units/g" It appears as though that the food itself contains the endotoxins, and any food exposed to bacteria, such as with fermentation, will have endotoxins. These endotoxins are resistant to heat as well as changes in ph typically found in the body as the
bacteria no longer have to be alive for endotoxins to be present. " LPS and BLP were found to be highly resistant to typical cooking times and
temperatures, low pH and protease treatment. In conclusion, apparently unspoiled foodstuffs can contain large quantities of stimulants of TLR2
and TLR4, both of which may regulate their capacity to stimulate inflammatory signalling." the authors finishing statements "Thus, it is tempting to speculate that the occasional ingestion of meals high in LPS and/or BLP could promote transient, mild, systemic inflammatory episodes that predispose subjects to the development of atherosclerosis and insulin resistance"
http://journals.cambridge.org/...
Citing again from the study previously mentioned titled Differential Effects of Cream, Glucose, and Orange Juice on Inflammation, Endotoxin, and the Expression of Toll-Like Receptor-4 and Suppressor of Cytokine Signaling-3
"Thus, saturated fats may have a more profound role in the pathogenesis of postprandial inflammation, as they may also perpetuate
inflammation through the increases in LPS and TLR-4."
http://www.ncbi.nlm.nih.gov/pm...
"The combined importance of dietary lipids and LPS in determining inflammatory risk may arise, since endotoxin has a strong affinity for chylomicrons (lipoproteins that transport dietary long-chain saturated fatty acids [SFAs] through the gut wall) as endotoxin crosses the gastrointestinal mucosa (23–25). As such, atherogenic and inflammatory risk may arise through a combination of dietary lipoprotein patterns and an increase in circulating endotoxin, exacerbated by feeding patterns (26,27). Therefore, altering the lipid profile through dietary
intervention may reduce endotoxin and the arising inflammatory response.... Finally, while the most obvious solution to metabolic endotoxinemia appears to be to reduce saturated fat intake, the Western diet is not conducive to this mode of action, and it is difficult for patients to comply with this request"
http://www.ncbi.nlm.nih.gov/pm...
To summarize, inflammation can be attributed to the consumption of endotoxins found in most animal products and the saturated fats found in
these foods act as pathways for the endotoxins. Since many chronic illnesses are attributed to this inflammation, what we need is to significantly lower intake of animal based foods.
This is merely a shred of the evidence against the use of animal products and it is abundant indeed. More studies from peer reviewed journals can be found on this website. Nutrition is not a philosophy, it is based on sound science.