US-Raised Meat

The Unsavory Truth of the McRib and Other Fake Foods, and Why Russia Banned US-Raised Meat

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By Dr. Mercola

Over the past couple of years, we’ve learned the unsavory truth about “pink slime,” reconstituted meat, and how the use of meat glue cheats you out of your hard-earned money at the grocery store and threatens your health.

We’ve also learned that fast food fare such as McDonald’s hamburgers contain so many chemicals and so few real food ingredients that a burger fails to show signs of decomposition after more than a decade…

The famous McDonald’s McRib also came under closer scrutiny, and turned out to be something less than mouthwatering. The McRib sandwich is a non-standard item on the fast food restaurant’s menu;1 its annual return is always advertised with great fanfare — last year it even made the headlines on ABC News.2

The pork sandwich is described as a tasty fan favorite slathered in tangy barbecue sauce, slivered onions and tart pickles, served on a hoagie style bun. Sounds perfectly normal, but what’s it made of, really? In a November 2011 article, CBS Chicago news3 spilled the beans on this seasonal favorite:

“More than 70 ingredients make up the McRib and, yes, one of them is pork. But as CBS 2’s Vince Gerasole reports, there’s also an ingredient that can be found in shoes… [Registered dietician Cassie] Vanderwall gave the McRib a closer look and found the McRib has azodicarbonamide, which is used to bleach the flour in bread. It has other uses. ‘It could be on your yoga mat, in your gym shoes, in your anything that’s rubbery,’ Vanderwall said…

Then there’s the pork – which is really restructured meat product. In other words, it’s made from all the less expensive innards and castoffs from the pig… Vanderwall said the McRib ingredient list ‘reminds me of a chemistry lab.’”

To see pictures of a ‘deconstructed’ McRib sandwich, check out foodfacts.info’s McRib page.4 It sure doesn’t look so appetizing anymore once the sauce is washed off and the meat sliced in half. In fact, it can barely pass meat, which was the point CBS news tried to make in the first place.

What is “Food” Anyway?

Two years ago, the nonprofit Physicians Committee for Responsible Medicine singled out McDonald’s in their advertisement against obesity-related deaths. As the ad claimed, obesity, diabetes, high cholesterol, hypertension and heart attacks are hallmark diseases associated with a fast food diet – a clear indication that it does not provide the appropriate nutrition for your body.

So, is McDonald’s fare really food?

When you consider the fact that a large number of the ingredients in a fast food meal exist nowhere in nature, but are rather concocted in a lab, the answer would have to be ‘no.’ Unfortunately, and to our severe detriment, ever since the advent of the so-called TV dinner back in the 1950’s, the concept of “food” has expanded from meat, vegetables, raw dairy products, fruit and other such natural items to include the highly processed, preserved, artificially flavored and often brightly colored chemical concoctions. But man simply was NOT designed to thrive on man-made chemicals.

Sadly, store-bought foods you might not recognize as processed, such as ground beef, are oftentimes no better. As reported last year, approximately 70 percent of the ground beef sold in U.S. supermarkets contains “pink slime” added in as a cheap filler.

The Pepto-Bismol-colored concoction consists of beef scraps and cow connective tissues, which has been treated with ammonium hydroxide (basically a solution of ammonia in water). It can legally make up 15 percent of any given beef product, which shaves about three cents off the cost for a pound of ground beef. The trimmings used come from parts of the cow that are most likely to be contaminated with dangerous bacteria like E. coli — which is why it must be treated with ammonia to kill off the pathogens in the first place. It’s really industrial food practices like this that pose very real threats to your health, not raw unpasteurized dairy products and other non-processed whole foods…

Russia Throws Poisonous Meat Back to U.S.

In related “questionable food” news, Russia has recently banned U.S. meat supplies after discovering it contains ractopamine — a beta agonist drug that increases protein synthesis, thereby making the animal more muscular. This reduces the fat content of the meat. As reported by Pravda,5 Russia is the fourth largest importer of US meats, purchasing about $500 million-worth of beef and pork annually.

The drug is banned for use in 160 countries, including China and Russia, but allowed in 24 countries, including Canada and the United States. According to the New York Times,6 the ban took effect as of December 7, 2012, and Russian health regulators stated that while they will initially conduct their own testing, foreign countries will soon be required to certify their meat as ractopamine-free if they want to export it to Russia. While the US Department of Agriculture (USDA) considers ractopamine safe and doesn’t test for it, Russia’s chief health inspector, Gennady Onishchenko, claims there are “serious questions” about the safety of the drug. He told the New York Times:

“For instance, use of ractopamine is accompanied by a reduction in body mass, suppression of reproductive function, increase of mastitis in dairy herds, which leads to a steep decline in the quality and safety of milk.”

Ractopamine is also known to affect the human cardiovascular system, and may cause food poisoning, according to Pravda.7 It’s also thought to be responsible for hyperactivity, muscle breakdown, and increased death and disability in livestock. While other drugs require a clearance period of around two weeks to help ensure the compounds are flushed from the meat prior to slaughter (and therefore reduce residues leftover for human consumption), there is no clearance period for ractopamine. In fact, livestock growers intentionally use the drug in the last days before slaughter in order to increase its effectiveness.

According to veterinarian Michael W. Fox, as much as 20 percent of ractopamine remains in the meat you buy from the supermarket. Despite potential health risks, the drug is used in 45 percent of U.S. pigs, 30 percent of ration-fed cattle, and an unknown percentage of turkeys.

Mexico and Brazil have announced that they will comply with Russia’s demand for ractopamine-free meats.8 The US has shown no sign of coming to an agreement, however. Instead the US has accused Russia of violating World Trade Organization (WTO) rules — an accusation Russian Deputy Prime Minister Arkady Dvorkovich has dismissed as being part of business as usual, since “all WTO members break these rules.”

How to Identify REAL Food

There are major incentives to center your diet on real foods as opposed to “food-like” products, the primary one being that real food is essential for optimal health. Real foods also taste delicious, and when bought from sustainable sources help to protect the environment. But with all the sneaky tricks being employed, how can you tell the difference? Here’s a listing of the characteristics and traits of real food versus processed “food products.”

Real Food Processed Food-Like Products
It’s grown, and sold “whole” Produced, manufactured in a factory, and sold in neat, convenient packages
Variable quality Always the same (no quality or taste variance)
Spoils fast Stays “fresh” for extended periods of time
Requires preparation No preparation required, just heat and serve
Vibrant colors and rich textures Contains fillers, additives and preservatives to make otherwise dull and bland mixtures appetizing
Authentically flavorful Artificially flavorful
Strong connection to land and culture No connection to land or culture
Shopping Guidelines for Real, Health-Promoting Food

As the U.S. agriculture industry now stands, antibiotics, pesticides, genetically engineered ingredients, hormones and countless drugs are fair game for inclusion in your food. So if you purchase your food from a typical supermarket, you’re taking the chance that your food is teeming with chemicals and drugs — even those that have been banned in other countries due to adverse health effects.

So please do your health a favor and support the small family farms in your area. You’ll receive nutritious food from a source that you can trust, and you’ll be supporting the honest work of a real family farm.

It all boils down to this: if you want to optimize your health, you must return to the basics of healthy food choices. Put your focus on WHOLE foods — foods that have not been processed or altered from their original state — food that has been grown or raised as nature intended, without the use of chemical additives, drugs, hormones, pesticides, fertilizers, and “mystery concoctions” of discarded scrap parts.

It’s really as simple as that!

And it’s not nearly as daunting a task as it may seem to find a local farmer that can supply your family with healthy, humanely raised animal products and produce. At LocalHarvest.org, for instance, you can enter your zip code and find farmers’ markets, family farms, and other sources of sustainably grown food in your area, all with the click of a button. Once you make the switch from supermarket to local farmer, the choice will seem natural, and you can have peace of mind that the food you’re feeding your family is naturally wholesome. That said, regardless of where you do your grocery shopping, these are the signs of high-quality, health-promoting foods you want to look for:

It’s grown without pesticides and chemical fertilizers (organic foods fit this description, but so do some non-organic foods)
It’s not genetically modified
It contains no added growth hormones, antibiotics, or other drugs
It does not contain any artificial ingredients, including chemical preservatives
It is fresh (keep in mind that if you have to choose between wilted organic produce or fresh conventional produce, the latter may actually be the better option)
It did not come from a factory farm
It is grown with the laws of nature in mind (meaning animals are fed their native diets, not a mix of grains and animal byproducts, and have free-range access to the outdoors)
It is grown in a sustainable way (using minimal amounts of water, protecting the soil from burnout, and turning animal wastes into natural fertilizers instead of environmental pollutants)
If the food meets these criteria, it is most likely a wise choice, and would fall under the designation of “real food.” Keep in mind that reclaiming your kitchen is part and parcel of healthful living, so you know exactly what you’re putting in your body. If you need help to get started, see Colleen Huber’s helpful tips on how to eat healthier organic food on a budget. And if you’re “hooked” on fast food and other processed foods, please review my article How to Wean Yourself Off Processed Foods in 7 Steps. It’s one of the absolute most positive life changes you could make!

Vitamin K

Vitamin K
From Wikipedia, the free encyclopedia
“Vitamin K” has also been used as a slang term for ketamine, an unrelated anaesthetic.
Vitamin K
Drug class
Use Vitamin K deficiency
Biological target Gamma-glutamyl carboxylase
ATC code B02BA
External links
MeSH D014812
AHFS/Drugs.com Medical Encyclopedia

Vitamin K1 (phylloquinone). Both forms of the vitamin contain a functional naphthoquinone ring and an aliphatic side-chain. Phylloquinone has a phytyl side-chain.

Vitamin K2 (menaquinone). In menaquinone, the side-chain is composed of a varying number of isoprenoid residues. The most common number of these residues is four, since animal enzymes normally produce menaquinone-4 from plant phylloquinone.

A sample of phytomenadione (vitamin K1) for injection. It is also called phylloquinone.
Vitamin K is a group of structurally similar, fat-soluble vitamins that are needed for the posttranslational modification of certain proteins required for blood coagulation and in metabolic pathways in bone and other tissue. They are 2-methyl-1,4-naphthoquinone (3-) derivatives. This group of vitamins includes two natural vitamers: vitamin K1 and vitamin K2.[1]
Vitamin K1, also known as phylloquinone, phytomenadione, or phytonadione, is synthesized by plants, and is found in highest amounts in green leafy vegetables because it is directly involved in photosynthesis. It may be thought of as the “plant form” of vitamin K. It is active in animals and may perform the classic functions of vitamin K in animals, including its activity in the production of blood clotting proteins. Animals may also convert it to vitamin K2.
Vitamin K2, the main storage form in animals, has several subtypes, which differ in isoprenoid chain length. These vitamin K2 homologs are called menaquinones, and are characterized by the number of isoprenoid residues in their side chains. Menaquinones are abbreviated MK-n, where M stands for menaquinone, the K stands for vitamin K, and the n represents the number of isoprenoid side chain residues. For example, menaquinone-4 (abbreviated MK-4) has four isoprene residues in its side chain. Menaquinone-4 (also known as menatetrenone from its four isoprene residues) is the most common type of vitamin K2 in animal products since it is normally synthesized from vitamin K1 in certain animal tissues (arterial walls, pancreas, and testes) by replacement of the phytyl tail with an unsaturated geranylgeranyl tail containing four isoprene units, thus yielding menaquinone-4. This homolog of vitamin K2 may have enzyme functions that are distinct from those of vitamin K1.
Bacteria in the colon (large intestine) can also convert K1 into vitamin K2. In addition, bacteria typically lengthen the isopreneoid side chain of vitamin K2 to produce a range of vitamin K2 forms, most notably the MK-7 to MK-11 homologs of vitamin K2. All forms of K2 other than MK-4 can only be produced by bacteria, which use these forms in anaerobic respiration. The MK-7 and other bacteria-derived form of vitamin K2 exhibit vitamin K activity in animals, but MK-7’s extra utility over menaquinone-4 (MK-4), if any, is unclear and is presently a matter of investigation.
Three synthetic types of vitamin K are known: vitamins K3, K4, and K5. Although the natural K1 and all K2 homologs have proven nontoxic, the synthetic form K3 (menadione) has shown toxicity.[2]

Contents [hide]
1 Discovery of vitamin K1
2 Conversion of vitamin K1 to vitamin K2 in animals
3 Subtypes of vitamin K2
4 Chemical structure
5 Physiology
6 Vitamin K absorption and dietary need
7 Recommended amounts
8 Anticoagulant drug interactions
9 Food sources
9.1 Vitamin K1
9.2 Vitamin K2
10 Deficiency
11 Toxicity
12 Biochemistry
12.1 Function
12.2 Gamma-carboxyglutamate proteins
12.3 Methods of assessment
12.4 Function in bacteria
13 Vitamin K injection in newborns
13.1 USA
13.2 UK
13.3 Controversy
14 Vitamin K and bone health
14.1 Vitamin K1 and bone health
14.2 Vitamin K2 (MK4) and bone health
14.3 Vitamin K2 (MK7) and bone health
15 Vitamin K and Alzheimer’s disease
16 Vitamin K used topically
17 Vitamin K and cancer
18 Vitamin K as antidote for poisoning by 4-hydroxycoumarin drugs
19 Vitamin K in rats
20 History of discovery
21 References
22 External links
[edit]Discovery of vitamin K1

Vitamin K1 (phylloquinone, phytomenadione, phytonadione) was identified in 1929 by Danish scientist Henrik Dam when he investigated the role of cholesterol by feeding chickens a cholesterol-depleted diet.[3] After several weeks, the animals developed hemorrhages and started bleeding. These defects could not be restored by adding purified cholesterol to the diet. It appeared that—together with the cholesterol—a second compound had been extracted from the food, and this compound was called the coagulation vitamin. The new vitamin received the letter K because the initial discoveries were reported in a German journal, in which it was designated as Koagulationsvitamin.
[edit]Conversion of vitamin K1 to vitamin K2 in animals

The MK-4 form of vitamin K2 is produced via conversion of vitamin K1 in the testes, pancreas and arterial walls.[4] While major questions still surround the biochemical pathway for the transformation of vitamin K1 to MK4, studies demonstrate the conversion is not dependent on gut bacteria, as it occurs in germ-free rats[5][6] and in parenterally-administered K1 in rats.[7][8] In fact, tissues that accumulate high amounts of MK4 have a remarkable capacity to convert up to 90% of the available K1 into MK4.[9][10] There is evidence that the conversion proceeds by removal of the phytyl tail of K1 to produce menadione as an intermediate, which is then condensed with an activated geranylgeranyl moiety (see also prenylation) to produce vitamin K2 in the MK-4 (menatetrione) form.[11].
[edit]Subtypes of vitamin K2

Main article: Vitamin K2
Vitamin K2 (menaquinone) includes several subtypes. The two subtypes most studied are menaquinone-4 (menatetrenone, MK4) and menaquinone-7 (MK7).
Menaquinone-7 (MK7) is different from MK4 in that it is not produced by human tissue. MK7 consumption has been shown to reduce the risk of bone fractures and cardiovascular disorders that are crucial health issues worldwide. There is a need for production of concentrated, supplementary MK7 in the diet.[citation needed] Recently, leading research teams from Australia, Japan and Korea are broadening the understandings on MK7 and its production. It has been reported that MK7 may be converted from phylloquinone (K1) in the colon by E-coli bacteria.[12] However, bacteria-derived menaquinones (MK7) appear to contribute minimally to overall vitamin K status.[13][14] MK4 and MK7 are both found in the United States in dietary supplements for bone health.
The US FDA has not approved any form of vitamin K for the prevention or treatment of osteoporosis; however, MK4 has been shown to decrease fractures up to 87%.[15] In the amount of 45 mg daily MK4 has been approved by the Ministry of Health in Japan since 1995 for the prevention and treatment of osteoporosis.[16]
Vitamin K2 (MK4, but not MK7 or vitamin K1) has also been shown to prevent bone loss and/or fractures in the following circumstances:
caused by corticosteroids (e.g., prednisone, dexamethasone, prednisolone),[17][18][19][20]
anorexia nervosa,[21]
cirrhosis of the liver,[22]
postmenopausal osteoporosis,[16][23][24][25][26][27]
disuse from stroke,[28]
Alzheimer’s disease,[29]
Parkinson disease,[30]
primary biliary cirrhosis[31]
and leuprolide treatment (for prostate cancer).[32]
[edit]Chemical structure

All members of the vitamin K group of vitamins share a methylated naphthoquinone ring structure (menadione), and vary in the aliphatic side chain attached at the 3-position (see figure 1). Phylloquinone (also known as vitamin K1) invariably contains in its side chain four isoprenoid residues, one of which is unsaturated.
Menaquinones have side chains composed of a variable number of unsaturated isoprenoid residues; generally they are designated as MK-n, where n specifies the number of isoprenoids.[33]
It is generally accepted that the naphthoquinone is the functional group, so that the mechanism of action is similar for all K-vitamins. Substantial differences may be expected, however, with respect to intestinal absorption, transport, tissue distribution, and bio-availability. These differences are caused by the different lipophilicity of the various side chains, and by the different food matrices in which they occur.
There are three synthetic forms of vitamin K, vitamins K3, K4, and K5, which are used in many areas including the pet food industry (vitamin K3) and to inhibit fungal growth (vitamin K5).[34]
[edit]Physiology

Vitamin K1, the precursor of most vitamin K in nature, is a steroisomer of phylloquinone, an important chemical in green plants, where it functions as an electron accepter in photosystem I during photosynthesis. For this reason, vitamin K1 is found in large quantities in the photosynthetic tissues of plants (green leaves, and dark green leafy vegetables such as romaine lettuce, kale and spinach), but it occurs in far smaller quantities in other plant tissues (roots, fruits, etc.). Iceberg lettuce contains relatively little. The function of phylloquinone in plants appears to have no resemblance to its later metabolic and biochemical function (as “vitamin K”) in animals, where it performs a completely different biochemical reaction.
Vitamin K (in animals) is involved in the carboxylation of certain glutamate residues in proteins to form gamma-carboxyglutamate (Gla) residues. The modified residues are often (but not always) situated within specific protein domains called Gla domains. Gla residues are usually involved in binding calcium, and are essential for the biological activity of all known Gla proteins.[35]
At this time, 15 human proteins with Gla domains have been discovered, and they play key roles in the regulation of three physiological processes:
Blood coagulation: prothrombin (factor II), factors VII, IX, and X, and proteins C, S, and Z[36]
Bone metabolism: osteocalcin, also called bone Gla protein (BGP), matrix Gla protein (MGP),[37] and periostin.[38]
Vascular biology: growth arrest-specific protein 6 (Gas6)[39]
Unknown function: proline-rich g-carboxy glutamyl proteins (PRGPs) 1 and 2, and transmembrane g-carboxy glutamyl proteins (TMGs) 3 and 4.[40]
Like other lipid-soluble vitamins (A, D, E), vitamin K is stored in the fat tissue of the human body.
[edit]Vitamin K absorption and dietary need

Previous theory held that dietary deficiency is extremely rare unless the intestine (small bowel) was heavily damaged, resulting in malabsorption of the molecule. The other at-risk group for deficiency were those subject to decreased production of K2 by normal flora, as seen in broad spectrum antibiotic use.[41] Taking broad-spectrum antibiotics can reduce vitamin K production in the gut by nearly 74% in people compared with those not taking these antibiotics.[42] Diets low in vitamin K also decrease the body’s vitamin K concentration.[43] Additionally, in the elderly there is a reduction in vitamin K2 production.[44]
Recent research results also demonstrate that the small intestine and large intestine (colon) seem to be inefficient at absorbing vitamin K.[45][46] These results are reinforced by human cohort studies, where a majority of the subjects showed inadequate vitamin K amounts in the body. This was revealed by the presence of large amounts of incomplete gamma-carboxylated proteins in the blood, an indirect test for vitamin K deficiency.[47][48][49] And in an animal model MK4 was shown to prevent arterial calcifications, pointing to its potential role in prevention of such calcification.[50] In this study vitamin K1 was also tested, in an attempt to make connections between vitamin K1 intake and calcification reduction. Only vitamin K2 (as MK4) was found to influence warfarin-induced calcification in this study.
[edit]Recommended amounts

The U.S. Dietary Reference Intake (DRI) for an Adequate Intake (AI) of vitamin K for a 25-year old male is 120 micrograms/day. The Adequate Intake (AI) for adult women is 90 micrograms/day, for infants is 10–20 micrograms/day, for children and adolescents 15–100 micrograms/day. In 2002 it was found that to get maximum carboxylation of osteocalcin, one may have to take up to 1000 μg of vitamin K1.[51]
[edit]Anticoagulant drug interactions

Phylloquinone (K1)[52][53] or menaquinone (K2) are capable of reversing the anticoagulant activity (incorrectly but colloquially referred to as “blood-thinning action”) of the powerful anticoagulant warfarin (tradename Coumadin). Warfarin works by blocking recycling of vitamin K, so that the body and tissues have lower levels of active vitamin K, and thus a deficiency of the active vitamin.
Supplemental vitamin K (for which oral dosing is often more active than injectable dosing in human adults) reverses the vitamin K deficiency caused by warfarin, and therefore modulates or totally reverses the intended anticoagulant action of warfarin and related drugs. Foods containing high amounts of vitamin K (green leafy vegetables) are avoided when taking warfarin. Sometimes small amounts of vitamin K (one milligram per day) are given orally to patients taking Coumadin so that the action of the drug is more predictable. The proper anticoagulant action of the drug is a function of vitamin K intake and drug dose, and (due to differing absorption) must be individualized for each patient. The action of warfarin and vitamin K both require two to five days after dosing to have maximum effect, and neither Coumadin or vitamin K shows much effect in the first 24 hours after they are given.
In two separate studies in the rat model, after long term administration of Coumadin to induce calcification of arteries in the rodents, supplemental vitamin K was found to reverse or prevent some of the arterial calcification attendant on the long-term blockade of vitamin K.[54] A second study found that only vitamin K2 as MK-4, and not vitamin K1 was effective at preventing warfarin-induced arterial calcification in rats, suggesting differing roles for the two forms of the vitamin in some calcium-dependent processes.[55]
The newer anticoagulant Pradaxa has a different mechanism of action that does not interact with vitamin K, and may be taken with supplemental vitamin K.[56]
[edit]Food sources

[edit]Vitamin K1
Food Serving Size Vitamin K1[57] Microgram (μg) Food Serving Size Vitamin K1[57] Microgram (μg)
Kale, cooked 1/2 cup 531 Parsley, raw 1/4 cup 246
Spinach, cooked 1/2 cup 444 Spinach, raw 1 cup 145
Collards, cooked 1/2 cup 418 Collards, raw 1 cup 184
Swiss chard, cooked 1/2 cup 287 Swiss chard, raw 1 cup 299
Mustard greens, cooked 1/2 cup 210 Mustard greens, raw 1 cup 279
Turnip greens, cooked 1/2 cup 265 Turnip greens, raw 1 cup 138
Broccoli, cooked 1 cup 220 Broccoli, raw 1 cup 89
Brussels sprouts, cooked 1 cup 219 Endive, raw 1 cup 116
Cabbage, cooked 1/2 cup 82 Green leaf lettuce 1 cup 71
Asparagus 4 spears 48 Romaine lettuce, raw 1 cup 57
Table from “Important information to know when you are taking: Warfarin (Coumadin) and Vitamin K”, Clinical Center, National Institutes of Health Drug Nutrient Interaction Task Force.[3]
Vitamin K1 is found chiefly in leafy green vegetables such as dandelion greens (which contain 778.4 μg per 100 g, or 741% of the recommended daily amount), spinach, swiss chard, and Brassica (e.g. cabbage, kale, cauliflower, broccoli, and brussels sprouts) and often the absorption is greater when accompanied by fats such as butter or oils; some fruits, such as avocado, kiwifruit and grapes, are also high in vitamin K. By way of reference, two tablespoons of parsley contain 153% of the recommended daily amount of vitamin K.[58] Some vegetable oils, notably soybean, contain vitamin K, but at levels that would require relatively large calorific consumption to meet the USDA-recommended levels.[59] Colonic bacteria synthesize a significant portion of humans’ vitamin K needs; newborns often receive a vitamin K shot at birth to tide them over until their colons become colonized at five to seven days of age from the consumption of their mother’s milk.
Phylloquinone’s tight binding to thylakoid membranes in chloroplasts makes it less bioavailable. For example, cooked spinach has a 5% bioavailability of phylloquinone, however, fat added to it increases bioavailability to 13% due to the increased solubility of vitamin K in fat.[60]
[edit]Vitamin K2
Main article: Vitamin K2
Food sources of vitamin K2 include fermented or aged cheeses, eggs, meats such as chicken and beef and their fat, livers, and organs, and in fermented vegetables, especially natto, as well as sauerkraut and kefir.[61]
Food 3 ½ ounce portion Microgram (μg) Proportion of vitamin K2 Food 3 ½ ounce portion Microgram (μg) Proportion of vitamin K2
Natto, cooked 1,103.4 (90% MK-7, 10% other MK) Chicken Leg 8.5 (100% MK-4)
Goose liver pâté 369.0 (100% MK-4) Ground beef (medium fat) 8.1 (100% MK-4)
Hard cheeses (Dutch Gouda style), raw 76.3 (6% MK-4, 94% other MK) Chicken liver (braised) 6.7 (100% MK-4)
Soft cheeses (French Brie style) 56.5 (6.5 MK-4, 93.5% other MK Hot dog 5.7 (100% MK-4)
Egg yolk, (Netherlands) 32.1 (98% MK-4, 2% other MK) Bacon 5.6 (100% MK-4)
Goose leg 31.0 (100% MK-4) Calf’s liver (pan-fried) 6.0 (100% MK-4)
Egg yolk (U.S.) 15.5 (100% MK-4) Sauerkraut 4.8 (100% MK-4)
Butter 15.0 (100% MK-4) Whole milk 1.0 (100% MK-4)
Chicken liver (raw) 14.1 (100% MK-4) Salmon (Alaska, Coho, Sockeye, Chum, and King wild (raw)) 0.5 (100% MK-4)
Chicken liver (pan-fried) 12.6 (100% MK-4) Cow’s liver (pan-fried) 0.4 (100% MK-4)
Cheddar cheese (U.S.) 10.2 (6% MK-4, 94% other MK) Egg white 0.4 (100% MK-4)
Meat franks 9.8 (100% MK-4) Skim milk 0.0
Chicken breast 8.9 (100% MK-4)
Table from “Rhéaume-Bleue, Kate. “Vitamin K2 and the Calcium Paradox” John Wiley & Sons Canada, Ltd., 2012, p. 66-67.
Vitamin K2 (menaquinone-4) is synthesized by animal tissues and is found in meat, eggs, and dairy products.[62] Menaquinone-7 is synthesized by bacteria during fermentation and is found in fermented soybeans (natto).[63] In natto, none of the vitamin K is from menaquinone-4, and in cheese only 2–7% is.[64]
[edit]Deficiency

Main article: Vitamin K deficiency
Average diets are usually not lacking in vitamin K, and primary deficiency is rare in healthy adults. Newborn infants are at an increased risk of deficiency. Other populations with an increased prevalence of vitamin K deficiency include those who suffer from liver damage or disease (e.g. alcoholics), cystic fibrosis, or inflammatory bowel diseases, or have recently had abdominal surgeries. Secondary vitamin K deficiency can occur in bulimics, those on stringent diets, and those taking anticoagulants. Other drugs associated with vitamin K deficiency include salicylates, barbiturates, and cefamandole, although the mechanisms are still unknown. Vitamin K1 deficiency can result in coagulopathy, a bleeding disorder.[64] Symptoms of K1 deficiency include anemia, bruising, and bleeding of the gums or nose in both sexes, and heavy menstrual bleeding in women.
Osteoporosis[65][66] and coronary heart disease[67][68] are strongly associated with lower levels of K2 (menaquinone). Vitamin K2 (MK-7) deficiency is also related to severe aortic calcification and all-cause mortality.[69] Menaquinone is not inhibited by salicylates as happens with K1, so menaquinone supplementation can alleviate the chronic vitamin K deficiency caused by long-term aspirin use.[citation needed]
[edit]Toxicity

Although allergic reaction from supplementation is possible, no known toxicity is associated with high doses of the phylloquinone (vitamin K1) or menaquinone (vitamin K2) forms of vitamin K, so no tolerable upper intake level (UL) has been set.[70]
Blood clotting (coagulation) studies in humans using 45 mg per day of vitamin K2 (as MK4)[27] and even up to 135 mg/day (45 mg three times daily) of K2 (as MK4),[71] showed no increase in blood clot risk. Even doses in rats as high as 250 mg/kg body weight did not alter the tendency for blood-clot formation to occur.[72]
Unlike the safe natural forms of vitamin K1 and vitamin K2 and their various isomers, a synthetic form of vitamin K, vitamin K3 (menadione), is demonstrably toxic. The FDA has banned this form from over-the-counter sale in the United States because large doses have been shown to cause allergic reactions, hemolytic anemia, and cytotoxicity in liver cells.[2]
[edit]Biochemistry

[edit]Function
The function of vitamin K1 in the cell is to add a carboxylic acid functional group to a glutamate amino acid residue in a proteins, to form a gamma-carboxyglutamate (Gla) residue. This is a somewhat uncommon post translational modification of the protein, which is then known as a “Gla protein.” The presense of two -COOH (carboxylate) groups on the same carbon in the gamma-carboxyglutamate residue allows it to chelate calcium ion. The binding of calcium ion in this way very often triggers the function or binding of Gla-protein enzymes, such as the so-called vitamin K dependent clotting factors discussed below.
Within the cell, vitamin K undergoes electron reduction to a reduced form called vitamin K hydroquinone by the enzyme vitamin K epoxide reductase (VKOR).[73] Another enzyme then oxidizes vitamin K hydroquinone to allow carboxylation of Glu to Gla; this enzyme is called the gamma-glutamyl carboxylase[74][75] or the vitamin K-dependent carboxylase. The carboxylation reaction will proceed only if the carboxylase enzyme is able to oxidize vitamin K hydroquinone to vitamin K epoxide at the same time; the carboxylation and epoxidation reactions are said to be coupled. Vitamin K epoxide is then reconverted to vitamin K by VKOR. The reduction and subsequent reoxidation of vitamin K coupled with carboxylation of Glu is called the vitamin K cycle.[76] Humans are rarely deficient in vitamin K1 because, in part, vitamin K 1 is continuously recycled in cells.[77]
Warfarin and other 4-hydroxycoumarins block the action of the VKOR.[78] This results in decreased concentrations of vitamin K and vitamin K hydroquinone in the tissues, such that the carboxylation reaction catalyzed by the glutamyl carboxylase is inefficient. This results in the production of clotting factors with inadequate Gla. Without Gla on the amino termini of these factors, they no longer bind stably to the blood vessel endothelium and cannot activate clotting to allow formation of a clot during tissue injury. As it is impossible to predict what dose of warfarin will give the desired degree of suppression of the clotting, warfarin treatment must be carefully monitored to avoid overdosing.
[edit]Gamma-carboxyglutamate proteins
At present, the following human Gla-containing proteins have been characterized to the level of primary structure: the blood coagulation factors II (prothrombin), VII, IX, and X, the anticoagulant proteins C and S, and the factor X-targeting protein Z. The bone Gla protein osteocalcin, the calcification-inhibiting matrix Gla protein (MGP), the cell growth regulating growth arrest specific gene 6 protein (Gas6), and the four transmembrane Gla proteins (TMGPs), the function of which is at present unknown. Gas6 can function as a growth factor to activate the Axl receptor tyrosine kinase and stimulate cell proliferation or prevent apoptosis in some cells. In all cases in which their function was known, the presence of the Gla residues in these proteins turned out to be essential for functional activity.
Gla proteins are known to occur in a wide variety of vertebrates: mammals, birds, reptiles, and fish. The venom of a number of Australian snakes acts by activating the human blood-clotting system. In some cases, activation is accomplished by snake Gla-containing enzymes that bind to the endothelium of human blood vessels and catalyze the conversion of procoagulant clotting factors into activated ones, leading to unwanted and potentially deadly clotting.
Another interesting class of invertebrate Gla-containing proteins is synthesized by the fish-hunting snail Conus geographus.[79] These snails produce a venom containing hundreds of neuroactive peptides, or conotoxins, which is sufficiently toxic to kill an adult human. Several of the conotoxins contain two to five Gla residues.[80]
[edit]Methods of assessment
Vitamin K status can be assessed by:
The prothrombin time (PT) test measures the time required for blood to clot. A blood sample is mixed with citric acid and put in a fibrometer; delayed clot formation indicates a deficiency. This test is insensitive to mild deficiency, as the values do not change until the concentration of prothrombin in the blood has declined by at least 50%.[81]
Undercarboxylated prothrombin (PIVKA-II), in a study of 53 newborns, found “PT (prothrombin time) is a less sensitive marker than PIVKA II”,[82] and as indicated above, PT is unable to detect subclinical deficiencies that can be detected with PIVKA-II testing.
Plasma phylloquinone was found to be positively correlated with phylloquinone intake in elderly British women, but not men,[83]
but an article by Schurges et al. reported no correlation between FFQ and plasma phylloquinone.[84]
Urinary γ-carboxyglutamic acid responds to changes in dietary vitamin K intake. Several days are required before any change can be observed. In a study by Booth et al., increases of phylloquinone intakes from 100 μg to between 377 and 417 μg for five days did not induce a significant change. Response may be age-specific.[85]
Undercarboxylated osteocalcin (UcOc) levels have been inversely correlated with stores of vitamin K[86] and bone strength in developing rat tibiae. Another study following 78 postmenopausal Korean women found a supplement regimen of vitamins K and D, and calcium, but not a regimen of vitamin D and calcium, was inversely correlated with reduced UcOc levels.[87]
[edit]Function in bacteria
Many bacteria, such as Escherichia coli found in the large intestine, can synthesize vitamin K2 (menaquinone-7),[88] but not vitamin K1 (phylloquinone). In these bacteria, menaquinone will transfer two electrons between two different small molecules, in a process called anaerobic respiration.[89] For example, a small molecule with an excess of electrons (also called an electron donor) such as lactate, formate, or NADH, with the help of an enzyme, will pass two electrons to a menaquinone. The menaquinone, with the help of another enzyme, will in turn transfer these two electrons to a suitable oxidant, such fumarate or nitrate (also called an electron acceptor). Adding two electrons to fumarate or nitrate will convert the molecule to succinate or nitrite + water, respectively. Some of these reactions generate a cellular energy source, ATP, in a manner similar to eukaryotic cell aerobic respiration, except the final electron acceptor is not molecular oxygen, but fumarate or nitrate. In aerobic respiration, the final oxidant is molecular oxygen (O2), which accepts four electrons from an electron donor such as NADH to be converted to water. E. coli can carry out aerobic respiration and menaquinone-mediated anaerobic respiration.
[edit]Vitamin K injection in newborns

The blood clotting factors of newborn babies are roughly 30 to 60% that of adult values; this may be due to the reduced synthesis of precursor proteins and the sterility of their guts. Human milk contains 1-4 μg/l of vitamin K1, while formula-derived milk can contain up to 100 μg/l in supplemented formulas. Vitamin K2 concentrations in human milk appear to be much lower than those of vitamin K1. Occurrence of vitamin K deficiency bleeding in the first week of the infant’s life is estimated at 0.25 to 1.7%, with a prevalence of two to 10 cases per 100,000 births.[90] Premature babies have even lower levels of the vitamin, so they are at a higher risk from this deficiency.
Bleeding in infants due to vitamin K deficiency can be severe, leading to hospitalizations, blood transfusions, brain damage, and death. Supplementation can prevent most cases of vitamin K deficiency bleeding in the newborn. Intramuscular administration is more effective in preventing late vitamin K deficiency bleeding than oral administration.[91][92]
[edit]USA
As a result of the occurrences of vitamin K deficiency bleeding, the Committee on Nutrition of the American Academy of Pediatrics has recommended 0.5 to 1.0 mg vitamin K1 be administered to all newborns shortly after birth.[92]
[edit]UK

This section does not cite any references or sources. Please help improve this section by adding citations to reliable sources. Unsourced material may be challenged and removed. (November 2011)
In the UK, vitamin K is administered to newborns as either a single injection at birth or three orally administered doses given at birth and then over the baby’s first month.
[edit]Controversy
Controversy arose in the early 1990s regarding this practice, when two studies suggested a relationship between parenteral administration of vitamin K and childhood cancer,[citation needed] however, poor methods and small sample sizes led to the discrediting of these studies, and a review of the evidence published in 2000 by Ross and Davies found no link between the two.[93][verification needed]
[edit]Vitamin K and bone health

Both physiological and observational evidence indicate vitamin K plays a role in bone growth and the maintenance of bone density, but efforts to delay the onset of osteoporosis by vitamin K supplementation have proven ineffective.
Vitamin K takes part in the post-translational modification as a cofactor in γ-carboxylation of vitamin K-dependant proteins (VKDPs). VKDPs have glutamate residues (Glu). Biophysical studies have suggested supplemental vitamin K promotes osteotrophic processes and slows osteoclastic processes via calcium bonding. Study of Atkins et al.[94] revealed phylloquinone, menatetrenone (MK4) and menadione promote in vitro mineralisaton by human primary osteoblasts. Other studies have shown vitamin K antagonists (usually a class of anticoagulants) lead to early calcification of the epiphysis and epiphysial line in mice and other animals, causing seriously decreased bone growth, due to defects in osteocalcin and matrix Gla protein. Their primary function is to prevent overcalcification of the bone and cartilage. Vitamin K is important in the process of carboxylating glutamic acid (Glu) in these proteins to gamma-carboxyglutamic acid (Gla), which is necessary for their function.[95][96] Vitamin D is reported to regulate the OC transcription by osteoblast thereby showing that vitamin K and vitamin D work in tandem for the bone metabolism and development. Lian and his group discovered two nucleotide substitution regions they named “osteocalcin box” in the rat and human osteocalcin genes.[97] They found a region 600 nucleotides immediately upstream from the transcription start site that support a 10-fold stimulated transcription of the gene by 1,25-dihydroxy vitamin D.
[edit]Vitamin K1 and bone health
Data from the 1998 Nurses Health Study, an observational study, indicated an inverse relationship between dietary vitamin K1 and the risk of hip fracture. After being given 110 micrograms/day of vitamin K, women who consumed lettuce one or more times per day had a significantly lower risk of hip fracture than women who consumed lettuce one or fewer times per week. In addition to this, high intakes of vitamin D but low intakes of vitamin K were suggested to pose an increased risk of hip fracture.[96][98] The Framingham Heart Study[99] is another study that showed a similar result. Subjects in the highest quartile of vitamin K1 intake (median K1 intake of 254 μg/ day) had a 35% lower risk of hip fracture than those in the lowest quartile. 254 μg/day is above the US Daily Reference Intake (DRI) of 90 μg/day for women and 120 μg/day for men. (See above)
In the face of this evidence, a large multicentre, randomized, placebo-controlled trial was performed to test the supplementation of vitamin K in postmenopausal women with osteopenia. Despite heavy doses of vitamin K1, no differences were found in bone density between the supplemented and placebo groups.[100]
[edit]Vitamin K2 (MK4) and bone health
MK4 has been shown in numerous studies to reduce fracture risk, and stop and reverse bone loss. In Japan, MK4 in the dose of 45 mg daily is recognized as a treatment for osteoporosis[98][101] under the trade name Glakay.[102] MK4 has been shown to decrease fractures up to 87%.[15] In the amount of 45 mg daily MK4 has been approved by the Ministry of Health in Japan since 1995 for the prevention and treatment of osteoporosis.[16]
MK4 (but not MK7 or vitamin K1) prevented bone loss and/or fractures in the following circumstances:
caused by corticosteroids (e.g., prednisone, dexamethasone, prednisolone)[17][18][19][20]
anorexia nervosa[21]
cirrhosis of the liver[22]
postmenopausal osteoporosis[16][23][24][25][26][27]
disuse from stroke[28]
Alzheimer’s disease[29]
Parkinson disease[30]
primary biliary cirrhosis[31]
leuprolide treatment (for prostate cancer).[32]
[edit]Vitamin K2 (MK7) and bone health
Menaquinone-7 (MK7), which is abundant in fermented soybeans (natto), has been demonstrated to stimulate osteoblastic bone formation and to inhibit osteoclastic bone resorption.[103] In another study, use of MK-7 caused significant elevations of serum Y-carboxylated osteocalcin concentration, a biomarker of bone formation. MK-7 also completely inhibited a decrease in the calcium content of bone tissue by inhibiting the bone-resorbing factors parathyroid hormone and prostaglandin E2.[104] On 19 February 2011, HSA (Singapore) approved a health supplement that contains vitamin K2 (MK7) and vitamin D3 for increasing bone mineral density.[105]
[edit]Vitamin K and Alzheimer’s disease

Research into the antioxidant properties of vitamin K indicates that the concentration of vitamin K is lower in the circulation of carriers of the APOE4 gene, and recent studies have shown its ability to inhibit nerve cell death due to oxidative stress. It has been hypothesized that vitamin K may reduce neuronal damage and that supplementation may hold benefits to treating Alzheimer’s disease, although more research is necessary in this area.[106]
[edit]Vitamin K used topically

Vitamin K may be applied topically, typically as a 5% cream, to diminish postoperative bruising from cosmetic surgery and injections, to treat broken capillaries (spider veins), to treat rosacea, and to aid in the fading of hyperpigmentation and dark under-eye circles.[107][108]
[edit]Vitamin K and cancer

While researchers in Japan were studying the role of vitamin K2 as the menaquinone-4 (MK-4) form in the prevention of bone loss in females with liver disease, they discovered another possible effect. This two-year study that involved 21 women with viral liver cirrhosis found that women in the supplement group were 90% less likely to develop liver cancer.[109][110] A German study performed on men with prostate cancer found a significant inverse relationship between vitamin K2 consumption and advanced prostate cancer.[111]
In 2006, a clinical trial showed that K2 as the menaquinone-4 (MK-4) (called menatetrenone in the study) might be able to reduce recurrence of liver cancer after surgery. It should be noted that this was a small pilot study and other similar studies did not show much effect. MK4 is now being tested along with other drugs to reduce liver cancer and has shown promising early results.[112]
[edit]Vitamin K as antidote for poisoning by 4-hydroxycoumarin drugs

Vitamin K is an antidote for poisoning by 4-hydroxycoumarin anticoagulant drugs (sometimes loosely referred to as coumarins). These include the pharmaceutical warfarin, and also anticoagulant-mechanism poisons such as bromadiolone, which are commonly found in rodenticides. 4-Hydroxycoumarin drugs possess anticoagulatory and rodenticidal properties because they inhibit recycling of vitamin K and thus cause simple deficiency of active vitamin K. This deficiency results in decreased vitamin K-dependent synthesis of some clotting factors by the liver. Death is usually a result of internal hemorrhage. Treatment for rodenticide poisoning usually consists of repeated intravenous doses of vitamin K, followed by doses in pill form for a period of at least two weeks, though possibly up to 2 months, after poisoning (this is necessary for the more potent 4-hydoxycoumarins used as rodenticides, which act by being fat-soluble and thus having a longer residence time in the body). If caught early, prognosis is good even when great amounts of the drug or poison are ingested, as these drugs are not true vitamin K antagonists, so the same amount of fresh vitamin K administered each day is sufficient for any dose of poison (although as noted, this must be continued for a longer time with more potent poisons). No matter how large the dose of these agents, they can do no more than prevent vitamin K from being recycled, and this metabolic problem may always be simply reversed by giving sufficient vitamin K (often 5 mg per day) to ensure that enough fresh vitamin K resides in the tissues to carry out its normal functions, even when efficient use of it by the body is prevented by the poison.
[edit]Vitamin K in rats

A recent study has shown that rats who are fed excess amounts of vitamin K had greater amounts of brain sulfatide concentrations.[113] This study indicates that vitamin K has more uses than originally thought, thus furthering the importance of daily vitamin K intake. The same study showed that a diet with insufficient vitamin K levels decreased the brain sulfatide concentrations in rats at the (p < . 01) significance level. Another study involving rats has indicated that different species, strains and genders of rats required different amounts of vitamin K intake, depending on how much was stored in their livers.[114] This may indicate that different humans should have different needs for their vitamin K intake. A third study looked at the way rats and chicks are able to recycle parts of vitamin K. The study found that chicks are about 10% less efficient in recycling the vitamin K than their rat counterparts.[115] This evidences also helps to confirm that vitamin K levels are unique to each species, and the previous study shows that required vitamin K intake also varies within species.
[edit]History of discovery

In 1929, Danish scientist Henrik Dam investigated the role of cholesterol by feeding chickens a cholesterol-depleted diet.[3] After several weeks, the animals developed hemorrhages and started bleeding. These defects could not be restored by adding purified cholesterol to the diet. It appeared that—together with the cholesterol—a second compound had been extracted from the food, and this compound was called the coagulation vitamin. The new vitamin received the letter K because the initial discoveries were reported in a German journal, in which it was designated as Koagulationsvitamin. Edward Adelbert Doisy of Saint Louis University did much of the research that led to the discovery of the structure and chemical nature of vitamin K.[116] Dam and Doisy shared the 1943 Nobel Prize for medicine for their work on vitamin K (K1 and K2) published in 1939. Several laboratories synthesized the compound(s) in 1939.[117]
For several decades, the vitamin K-deficient chick model was the only method of quantifying vitamin K in various foods: the chicks were made vitamin K-deficient and subsequently fed with known amounts of vitamin K-containing food. The extent to which blood coagulation was restored by the diet was taken as a measure for its vitamin K content. Three groups of physicians independently found this: Biochemical Institute, University of Copenhagen (Dam and Johannes Glavind), University of Iowa Department of Pathology (Emory Warner, Kenneth Brinkhous, and Harry Pratt Smith), and the Mayo Clinic (Hugh Butt, Albert Snell, and Arnold Osterberg).[118]
The first published report of successful treatment with vitamin K of life-threatening hemorrhage in a jaundiced patient with prothrombin deficiency was made in 1938 by Smith, Warner, and Brinkhous.[119]
The precise function of vitamin K was not discovered until 1974, when three laboratories (Stenflo et al.,[120] Nelsestuen et al.,[121] and Magnusson et al.[122]) isolated the vitamin K-dependent coagulation factor prothrombin (Factor II) from cows that received a high dose of a vitamin K antagonist, warfarin. It was shown that, while warfarin-treated cows had a form of prothrombin that contained 10 glutamate amino acid residues near the amino terminus of this protein, the normal (untreated) cows contained 10 unusual residues that were chemically identified as gamma-carboxyglutamate, or Gla. The extra carboxyl group in Gla made clear that vitamin K plays a role in a carboxylation reaction during which Glu is converted into Gla.
The biochemistry of how vitamin K is used to convert Glu to Gla has been elucidated over the past thirty years in academic laboratories throughout the world.

Vegetarian Diet

Introduction
The term “vegetarian” is used to describe any diet that emphasizes the consumption of plant foods and discourages the consumption of animal foods. In its most restrictive form, a vegetarian diet excludes all animal foods, including animal flesh, dairy products and eggs. Vegan, macrobiotic, and fruitarian diets fall into this category. Less restrictive forms include the lacto-ovo vegetarian diet (includes dairy products and eggs) and the lacto-vegetarian diet (includes dairy products). The popularity of vegetarianism is on the rise in the United States, and converts cite personal health, spiritual and religious beliefs, concern about animal welfare, and distress about the economic and environmental consequences of a meat-based diet as reasons for adopting a plant-based diet. This movement towards vegetarianism is consistent with a growing body of research that touts the health benefits of plant-based diets including lower rates of obesity, hypertension, diabetes, arthritis, colon cancer, prostate cancer, and heart disease. When carefully planned and well-balanced, vegetarian diets provide sufficent amounts of all essential nutrients. However, because infants, children, adolescents, and pregnant and lactating women have increased caloric and nutrient needs, care must be taken to include a variety of foods from all food groups (fruits, vegetables, legumes, nuts, seeds, and, for those vegetarians who consume them, eggs and/or dairy products) to ensure that nutritional needs are met.

History
Throughout human history, advocates of vegetarianism have employed moral and spiritual arguments to express their disdain for eating the flesh of animals. Ancient writers such as Ovid and Plutarch deplored the killing of innocent creatures for food. Plutarch stated: “I am astonished to think what appetite first induced man to taste of a dead carcass or what motive could suggest the notion of nourishing himself with the flesh of animals which he saw, just before, bleating, bellowing, walking, and looking about them.” The Greek philosopher Pythagoras, who lived towards the end of the 6th century BC, argued that the flesh of beasts contaminated and brutalized the soul. In recognition of Pythagoras’ commitment, vegetarians were known as Pythagoreans until the mid-19th century. Other writers have associated vegetarianism with spiritual enlightenment. According to the 17th century English vegetarian Thomas Tryon, “…by thoroughly cleansing the outward court of terrestrial nature, it opens the windows of the inward senses of the soul.” (Whorton, 1994) For these reasons, a variety of religions, including Brahminism, Buddhism, Hinduism and the Seventh Day Adventists encourage followers to abstain from eating meat.

While philosophers have long articulated the moral and spiritual benefits of the vegetarian way of life, the pursuit of vegetarianism for the reasons of health did not begin until the 19th Century. Early in the 1800s, scientific and medical evidence for the benefits of plant-based diets began to emerge. In 1806, a London physician named William Lambe cured himself of longstanding illness by abstaining from meat. Encouraged by his experience, Lambe began to treat his patients with the same diet prescription. His work eventually convinced many of his colleagues that a plant-based diet was as, or more healthy than a meat-based diet. Around the same time in the United States, a popular health reform movement was gathering steam. This movement was initiated by Presbyterian minister Sylvester Graham, most well-known now as the father of the Graham cracker. Graham, who preached on temperance and denounced the growing use of refined flour, was also a vegetarian. Following the establishment of the British Vegetarian Society in 1847, Graham worked to organize a similar group in America, and the American Vegetarian Society was founded in 1850. In the late 1800s, John Harvey Kellog, a Seventh Day Adventist and the maker of cereals bearing his family name, labored to make Americans aware of the nutritional benefits of vegetarianism.

During the 19th and 20th centuries, scientists continued to evaluate the health benefits of vegetarian diets. But, even as a growing body of scientific evidence emerged to validate this way of life, vegetarianism remained, to a large extent, on the fringe of society. Even as late as the 1970s, vegetarianism was associated with the counter-culture, a diet adhered to only by flower children and religious fanatics.

Popularity
During the last few decades of the 20th Century, the popularity of vegetarianism surged in the United States and Europe, as evidenced by the number of people claiming to be vegetarian and the increase in published literature promoting the health benefits of vegetarian diets. According to one source, in 1994 more than 12 million people in the United States reported themselves to be vegetarians, compared to 6 million in 1986 (Rajaram and Sabate, 2000). The Vegetarian Resource Group, a leading source of information on vegetarianism, reported the results of a 2000 survey that estimated the number of vegetarians in the United States to be only about 5 million people. In Europe, it is estimated that 5% of the populations of both the United Kingdom and Germany are vegetarian, and 4% of the adult population of the Netherlands follows a vegetarian diet (Hebbelinck, 1999). Vegetarians cite personal health, spiritual and religious beliefs, concern about animal welfare, and distress over the economic and environmental consequences of a meat-based diet as reasons for adopting a plant-based diet.

Are you a vegetarian? If so, you are in good company! Famous vegetarians include Mahatma Ghandi, Carl Lewis (Olympic athlete), Natalie Merchant (musician); Vanessa Williams (actress and singer); Raffi (children’s musician); Dean Ornish, MD (cardiologist and author); Paul McCartney (rock musician); Desmond Howard (Heisman trophy winner); Dustin Hoffman (actor); Tony LaRussa (pro-baseball manager); and Fred Rogers (TV’s Mr. Rogers).

Principles
In general, the term “vegetarian” is used to describe any diet that emphasizes the consumption of plant foods, avoids the consumption of animal flesh, and discourages the consumption of other animal products. In its most restrictive form, a vegetarian diet excludes all animal foods, including animal flesh, dairy products and eggs. Vegan, macrobiotic, and fruitarian diets fall into this category. Less restrictive forms include the lacto-ovo vegatarian diet (includes dairy products and eggs) and the lacto-vegetarian diet (includes dairy products). Interestingly, many people who claim to be “vegetarian” do not fit into any of the categories above. Many who consider themselves vegetarian eat fish on occasion, while other self-defined vegetarians include poultry and/or pork in their diet.

To be considered healthy, a vegetarian diet should include daily consumption of a variety of foods from all the plant groups, such as grains, legumes, vegetables, fruit, nuts, seeds, plant oils, herbs and spices. To maximize the nutritional value of their diet, vegetarians should choose whole, organic, minimally processed foods, and go easy on highly processed foods, junk foods and sweets. A vegetarian diet featuring lots of chips, cookies and frozen confections, even if made from organic ingredients, will not promote health.

Research
A significant body of population-based research documents the health benefits of a vegetarian diet. For example, a paper published in 1999 summarized the results of a study associating diet with chronic disease in a group of nearly 35,000 Seventh day Adventists living in California. The members of the group who followed a vegetarian diet (defined as eating no red meat, poultry, or fish)had lower incidences of many diseases, including obesity, hypertension, diabetes, arthritis, colon cancer, prostate cancer, and ischemic heart disease than the nonvegetarians (Fraser, 1999). Also in 1999, Key, et al., analyzed the combined results from five studies involving a total of more than 76,000 people that compared the incidence of disease among vegetarians (defined as eating no red meat, poultry or fish) to that of nonvegetarians with similar lifestyles. Mortality from ischemic heart disease was 24% lower in vegetarians than nonvegetarians (Key, et al).

For many years, the health benefits of vegetarian diets were thought to be due to the absence of meat and other animal fats in the diet, and the subsequent reduction in the intake of several known dietary villains such as total fat, saturated fat and cholesterol. In support of this explanation, scientists pointed to results of research studies that link high intake of the above-mentioned dietary villains to an increased risk for various medical conditions including heart disease and cancer. Researchers have also suggested that the health benefits of vegetarian diets are due, at least in part, to other healthy lifestyle choices that often accompany vegatarianism, such as increased physical activity and not smoking.

Clearly, avoiding meat and animal fats and increasing physical activity contribute to the health benefits of a vegetarian lifestyle. However, recent research has focused on the presence of a variety of specific nutrients in plant foods that have health-promoting qualities.

Fiber: Plant foods such as whole grains, beans, legumes, fruits, vegetables, and nuts provide dietary fiber. High intake of dietary fiber may reduce your risk of developing heart disease, diabetes, premenstrual syndrome, and colon cancer.
Antioxidants: Fruits and vegetables contain high amounts of vitamin C, vitamin E, and carotenoids, all of which act as antioxidants, protecting your cells from the damaging effects of free radicals
Phytonutrients: Plant foods contain a variety of unique nutrients such as phytoestrogens, indoles, isothiocyanates, and flavonoids. Emerging research indicates that these nutrients may help prevent cancer, heart disease, and other degenerative diseases.
Advocates of vegetarianism also point to research on the environmental impact of meat-based diets to support their lifestyle. Consider these facts:

Thirty-eight percent of total grain production worldwide is fed to chicken, pigs, and cattle. Seventy percent of grain production in the United States is fed to livestock. (Gussow, 1994)
The United States is losing approximately 4 million acres of cropland each year due to soil erosion. It is estimated that 85% of this topsoil loss is directly related to raising livestock. (The Vegetarian Times Complete Cookbook, 1995)
More than 4,000 gallons of water are needed to produce a single day’s worth of food for the typical meat eater. In comparison, an ovo-lacto vegetarian requires only 1,200 gallons of water, and a vegan needs a mere 300 gallons. (The Vegetarian Times Complete Cookbook, 1995)
One pound of pork that provides between 1000 and 2000 calories takes 14,000 calories of energy to produce in the United States. (Gussow, 1994)
Huge livestock farms generate an estimated five tons of animal manure for every person in the United States. In one day, a single hog farm produces the same amount of raw waste as a city of 12,000 people. In one year, a large egg farm yields enough manure to fill 1,400 dump trucks. Manure from livestock farms pollutes rivers and lakes, resulting in overgrowth of algae and pathogenic (disease-causing) microorganisms.
In Latin America, 20 million hectares of tropical forest have been converted to cattle pasture since 1970. This deforestation has had a devastating impact on plant and animal diversity in Latin America. (Gussow, 1994)
Many medical authorities link the emergence of foodborne pathogens such as E.coli and Mad Cow disease with factory farming methods.
One-third of the irrigation water in the State of California is used to produce feed for dairy cattle.
Foods Emphasized
Vegetarian diets emphasize the consumption of grains, vegetables, fruits, beans, soy products, nuts, and seeds.

Foods Avoided
All true vegetarian diets exclude meat, fish, and poultry. Strict vegetarian diets also exclude dairy products and eggs, while more liberal vegetarian diets include dairy products and eggs.

Nutrient Excesses/Deficiencies
Historically, vegetarian diets have been condemned by nutritionists for providing inadequate amounts of several important nutrients that are found primarily in animal foods including iron, protein, calcium, vitamin D, and vitamin B12. However, it is now widely accepted by most nutritionists that vegetarian diets, when a variety of plant foods are included, can meet or exceed the nutritional requirements of most individuals.

Although vegetarian diets do tend to be lower in iron than meat-based diets, vegetarians do not have a higher rate of iron deficiency anemia than meat eaters. This may be explained by the fact that the iron found in vegetarian diets (in vegetables and unrefined grains) is often accompanied, in the food or in the meal, by large amounts of vitamin C, which increases the absorption of the mineral.

Vegetarians also tend to eat less protein than meat-eaters, but their intake still exceeds the required amounts. Several decades ago, it was believed that vegetarians had to eat complementary proteins at each meal to ensure adequate intake of all the essential amino acids. It is now known that vegetarians need not worry about complementary proteins at each meal, as long as they ensure intake of foods containing all essential amino acids during the day. For more information on complementary proteins, see the article on protein in our nutrient database.

Since vitamin D-fortified milk is the primary food source of vitamin D in the United States, vegetarians who exclude dairy products from their diet may require a supplemental source, especially if they do not have consistent exposure to the sun.

As is the case with vitamin D, the calcium intake of vegetarians depends to a great extent on whether or not dairy products are included in the diet. All vegetarians should incorporate plant foods (dark green leafy vegetables and organic tofu) that contain calcium, but this is especially important for those who exclude dairy products. Interestingly, because vegetarian diets tend to be lower in protein, vegetarians may retain more calcium than meat-eaters, thus promoting bone health.

Vegans must pay attention to their intake of vitamin B12 since this vitamin occurs primarily in animal foods, and its deficiency can cause a variety of irreversible neurological problems. A study published in 1999 involving 245 Australian Seventh-day Adventist ministers evaluated the vitamin B12 status of lactovo-vegetarianns and vegans who were not taking vitamin B12 supplements. Seventy three percent of the participants had low serum vitamin B12 concentrations. (Hokin, 1999) Interestingly, vitamin B12 cannot be made by animals or plants, but only by microorganisms, like bacteria. When plant foods are fermented with the use of B12-producing bacteria, they end up containing B12. Otherwise, they usually don’t. Sea plants are an exception to the fermented plant rule since they can contain small amounts of B12 from contact with microorganisms in the ocean. Although animals cannot make vitamin B12, they are able to store B12 in their liver and muscles. The storage of B12 by animals explains why animal foods are the primary food sources of dietary B12.

Another nutrient to which vegetarians should pay special attention is docosahexaenoic acid (DHA). DHA is an omega 3 fatty acids believed to play an important role in the development and function of the central nervous system, as well as the eyes. It occurs naturally in meat, fish, eggs, and milk. DHA an also be synthesized by the body from alpha-linolenic acid, an omega 3 essential fatty acid, although it is not yet clear to what extent this conversion actually takes place. This process is slowed by the presence of large amounts of another essential fatty acid called linoleic acid, which is an omega 6 fat found in corn, safflower and sunflower oils. Vegetarians, and especially vegans, may want to supplement with DHA. To maintain a beneficial ratio of omega 3 fatty acids to omega 6 fatty acids, they may also want to and/or substitute foods containing alpha-linolenic acid, such as flaxseeds, pumpkin seeds and soybeans for foods containing linoleic acid.

Who Benefits
A vegetarian diet may be especially beneficial for overweight individuals, as well as for women with premenstrual syndrome and individuals with diabetes, high blood pressure and/or cardiovascular disease.

Who is Harmed
Because infants, children, adolescents, and pregnant and lactating women have increased caloric and nutrient needs, individuals in any of these groups choosing to follow a vegetarian diet must take care to include a variety and adequate amount of food from all food groups (fruits, vegetables, grains, legumes, nuts, and seeds) to ensure that nutritional needs are met.

Menu Ideas
These vegetarian recipes were developed by the George Mateljan Foundation.

Resources
For additional information about vegetarianism, contact the following organizations:

Earthsave
http://www.earthsave.org
The North American Vegetarian Society
P.O. Box 72
Dolgeville, NY 13329
Phone: 518-568-7970
Vegetarian Resource Center
P.O. Box 38-1068
Cambridge, MA 02238
Phone: 617-625-3790
The Vegetarian Resource Group
P.O. Box 1463
Baltimore, MD 21203
Phone: 410-366-8343
References
Beilin LJ. Vegetarian and other complex diets, fats, fiber, and hypertension. Am J Clin Nutr 1994; 59(suppl): 1130S-5S. 1994.
Craig WJ. Iron status of vegetarians. Am J Clin Nutr 1994; 59(suppl): 1233S-7S. 1994.
Editors of Vegetarian Times. Vegetarian Times Complete Cookbook. Macmillan: New York, 1995. 1995.
Fraser GE. Associations between diet and cancer, ischemic heart disease, and all-cause mortality in non-Hispanic white California Seventh-day Adventists. Am J Clin Nutr 1999; 70(suppl): 532S-8S. 1999.
Gibson RS. Content and bioavailability of trace elements in vegetarian diets. Am J Clin Nutr 1994; 59(suppl): 1223S-32S. 1994.
Gussow JD. Ecology and vegetarian considerations: does environmental responsibility demand the elimination of livestock?. Am J Clin Nutr; 59(suppl): 1110S-6S. 0.
Haddad EH, Sabate J, Whitten CG. Vegetarian food guide pyramid: a conceptual framework. Am J Clin Nutr 1999; 70(suppl): 615S-9S. 1999.
Hebbelinck M, Clarys P, de Malsche A. Growth, development, and physical fitness of Flemish vegetarian children, adolescents and young adults. Am J Clin Nutr 1999; 70(suppl): 579S-85S. 1999.
Herbert V. Staging vitamin B-12 (cobalamin) status in vegetarians. Am J Clin Nutr 1994; 59(suppl): 1213S-22S. 1994.
Hokin BD, Butler T. Cyanocobalamin (vitamin B-12) status in Seventh-day Adventist ministers in Australia. Am J Clin Nutr 1999; 70(suppl): 576S-8S. 1999.
Key TJ, et al. Mortality in vegetarians and nonvegetarians: detailed findings from a collaborative analysis of 5 prospective studies. Am J Clin Nutr 1999; 70(suppl): 516S-24S. 1999.
Rajaram S, Sabate J. Health benefits of a vegetarian diet. Nutrition 2000; 16: 531-533. 2000.
Sanders TAB, Reddy S. Vegetarian diets and children. Am J Clin Nutr 1994; 59(suppl):1176S-81S. 1994.
Weaver CM, Plawecki KL. Dietary calcium: adequacy of a vegetarian diet. Am J Clin Nutr 1994; 59(suppl): 1238S-41S. 1994.
Whorton JC. Historical development of vegetarianism. Am J Clin Nutr 1994; 59(suppl): 1103S-9S. 1994.
Willett WC. Convergence of philosophy and science: the Third International Congress on Vegetarian Nutrition. Am J Clin Nutr 1999; 79(suppl): 434S-8S. 1999.

What is Cholesterol?

What is Cholesterol? What Causes High Cholesterol?

Cholesterol is a lipid (fat) which is produced by the liver. Cholesterol is vital for normal body function. Every cell in our body has cholesterol in its outer layer.

Cholesterol is a waxy steroid and is transported in the blood plasma of all animals. It is the main sterol synthesized by animals – small amounts are also synthesized in plants and fungi. A sterol is a steroid sub-group.

Cholesterol levels among US adults today are generally higher than in all other industrial nations. During the 1990s there was some concern about cholesterol levels in American children. According to the CDC (Centers for Disease Control and Prevention), nearly 1 in every 10 children/adolescents in the USA has elevated total cholesterol levels; and this was after concentrations had dropped over a 20-year period.

The word “cholesterol” comes from the Greek word chole, meaning “bile”, and the Greek word stereos, meaning “solid, stiff”.
What are the functions of cholesterol?

It builds and maintains cell membranes (outer layer), it prevents crystallization of hydrocarbons in the membrane
It is essential for determining which molecules can pass into the cell and which cannot (cell membrane permeability)
It is involved in the production of sex hormones (androgens and estrogens)
It is essential for the production of hormones released by the adrenal glands (cortisol, corticosterone, aldosterone, and others)
It aids in the production of bile
It converts sunshine to vitamin D. Scientists from the Rockefeller University were surprised to find that taking vitamin D supplements do not seem to reduce the risk of cholesterol-related cardiovascular disease.
It is important for the metabolism of fat soluble vitamins, including vitamins A, D, E, and K
It insulates nerve fibers
There are three main types of lipoproteins

Cholesterol is carried in the blood by molecules called lipoproteins. A lipoprotein is any complex or compound containing both lipid (fat) and protein. The three main types are:
LDL (low density lipoprotein) – people often refer to it as bad cholesterol. LDL carries cholesterol from the liver to cells. If too much is carried, too much for the cells to use, there can be a harmful buildup of LDL. This lipoprotein can increase the risk of arterial disease if levels rise too high. Most human blood contains approximately 70% LDL – this may vary, depending on the person.

HDL (high density lipoprotein) – people often refer to it as good cholesterol. Experts say HDL prevents arterial disease. HDL does the opposite of LDL – HDL takes the cholesterol away from the cells and back to the liver. In the liver it is either broken down or expelled from the body as waste.

Triglycerides – these are the chemical forms in which most fat exists in the body, as well as in food. They are present in blood plasma. Triglycerides, in association with cholesterol, form the plasma lipids (blood fat). Triglycerides in plasma originate either from fats in our food, or are made in the body from other energy sources, such as carbohydrates. Calories we consume but are not used immediately by our tissues are converted into triglycerides and stored in fat cells. When your body needs energy and there is no food as an energy source, triglycerides will be released from fat cells and used as energy – hormones control this process.
What are normal cholesterol levels?

The amount of cholesterol in human blood can vary from 3.6 mmol/liter to 7.8 mmol/liter. The National Health Service (NHS), UK, says that any reading over 6 mmol/liter is high, and will significantly raise the risk of arterial disease. The UK Department of Health recommends a target cholesterol level of under 5 mmo/liter. Unfortunately, two-thirds of all UK adults have a total cholesterol level of at least five (average men 5.5, average women 5.6).

Below is a list of cholesterol levels and how most doctors would categorize them in mg/dl (milligrams/deciliter) and 5mmol/liter (millimoles/liter).
Desirable – Less than 200 mg/dL
Bordeline high – 200 to 239 mg/dL
High – 240 mg/dL and above

Optimum level: less than 5mmol/liter
Mildly high cholesterol level: between 5 to 6.4mmol/liter
Moderately high cholesterol level: between 6.5 to 7.8mmol/liter
Very high cholesterol level: above 7.8mmol/liter
Dangers of high cholesterol levels

High cholesterol levels can cause:
Atherosclerosis – narrowing of the arteries.

Higher coronary heart disease risk – an abnormality of the arteries that supply blood and oxygen to the heart.

Heart attack – occurs when the supply of blood and oxygen to an area of heart muscle is blocked, usually by a clot in a coronary artery. This causes your heart muscle to die.

Angina – chest pain or discomfort that occurs when your heart muscle does not get enough blood.

Other cardiovascular conditions – diseases of the heart and blood vessels.

Stroke and mini-stroke – occurs when a blood clot blocks an artery or vein, interrupting the flow to an area of the brain. Can also occur when a blood vessel breaks. Brain cells begin to die.
If both blood cholesterol and triglyceride levels are high, the risk of developing coronary heart disease rises significantly.

Symptoms of high cholesterol (hypercholesterolaemia)

Symptoms of high cholesterol do not exist alone in a way a patient or doctor can identify by touch or sight. Symptoms of high cholesterol are revealed if you have the symptoms of atherosclerosis, a common consequence of having high cholesterol levels. These can include:
Narrowed coronary arteries in the heart (angina)

Leg pain when exercising – this is because the arteries that supply the legs have narrowed.

Blood clots and ruptured blood vessels – these can cause a stroke or TIA (mini-stroke).

Ruptured plaques – this can lead to coronary thrombosis (a clot forming in one of the arteries that delivers blood to the heart). If this causes significant damage to heart muscle it could cause heart failure.

Xanthomas – thick yellow patches on the skin, especially around the eyes. They are, in fact, deposits of cholesterol. This is commonly seen among people who have inherited high cholesterol susceptibility (familial or inherited hypercholesterolaemia).
What causes high cholesterol?

Lifestyle causes
Nutrition – although some foods contain cholesterol, such as eggs, kidneys, eggs and some seafoods, dietary cholesterol does not have much of an impact in human blood cholesterol levels. However, saturated fats do! Foods high in saturated fats include red meat, some pies, sausages, hard cheese, lard, pastry, cakes, most biscuits, and cream (there are many more).

Sedentary lifestyle – people who do not exercise and spend most of their time sitting/lying down have significantly higher levels of LDL (bad cholesterol) and lower levels of HDL (good cholesterol).

Bodyweight – people who are overweight/obese are much more likely to have higher LDL levels and lower HDL levels, compared to people who are of normal weight.

Smoking – this can have quite a considerable effect on LDL levels.

Alcohol – people who consume too much alcohol regularly, generally have much higher levels of LDL and much lower levels of HDL, compared to people who abstain or those who drink in moderation.
Treatable medical conditions

These medical conditions are known to cause LDL levels to rise. They are all conditions which can be controlled medically (with the help of your doctor, they do not need to be contributory factors):
Diabetes
High blood pressure (hypertension)
High levels of triglycerides
Kidney diseases
Liver diseases
Under-active thyroid gland
Risk factors which cannot be treated

These are known as fixed risk factors:
Your genes 1 – people with close family members who have had either a coronary heart disease or a stroke, have a greater risk of high blood cholesterol levels. The link has been identified if your father/brother was under 55, and/or your mother/sister was under 65 when they had coronary heart disease or a stroke.

Your genes 2 – if you have/had a brother, sister, or parent with hypercholesterolemia (high cholesterol) or hyperlipidemia (high blood lipids), your chances of having high cholesterol levels are greater.

Your sex – men have a greater chance of having high blood cholesterol levels than women.

Your age – as you get older your chances of developing atherosclerosis increase.

Early menopause – women whose menopause occurs early are more susceptible to higher cholesterol levels, compared to other women.

Certain ethnic groups – people from the Indian sub-continent (Pakistan, Bangladesh, India, Sri Lanka) are more susceptible to having higher cholesterol levels, compared to other people.
How is high cholesterol diagnosed?

Blood and cholesterol screening results Cholesterol levels may be measured by means of a simple blood test. It is important not to eat anything for at least 12 hours before the blood sample is taken. The blood sample can be obtained with a syringe, or just by pricking the patient’s finger.

The blood sample will be tested for LDL and HDL levels, as well as blood triglyceride levels. The units are measure in mg/dl (milligrams/deciliter) or 5mmol/liter (millimoles/liter).

Researchers at the Sree Sastha Institute of Engineering and Technology, India, developed a photographic cholesterol test, which they describe as a completely non-invasive way to test cholesterol levels.

People who have risk factors should consider having their cholesterol levels checked.
What are the treatments for high cholesterol?

Lifestyle

Most people, especially those whose only risk factor has been lifestyle, can generally get their cholesterol and triglyceride levels back to normal by:
Doing plenty of exercise (check with your doctor)
Eating plenty of fruits, vegetables, whole grains, oats, good quality fats
Avoiding foods with saturated fats .In general, the main sources of saturated fat are from animal products: red meat and whole-milk dairy products, including cheese, sour cream, ice cream and butter.
Getting plenty of sleep (8 hours each night)
Bringing your bodyweight back to normal
Avoiding alcohol
Stopping smoking
Many experts say that people who are at high risk of developing cardiovascular disease will not lower their risk just by altering their diet. Nevertheless, a healthy diet will have numerous health benefits.

Cholesterol-controlling medications

If your cholesterol levels are still high after doing everything mentioned above, your doctor may prescribe a cholesterol-lowering drug. They may include the following:
Statins (HMG-CoA reductase inhibitors) – these block an enzyme in your liver that produces cholesterol. The aim here is to reduce your cholesterol levels to under 4 mmol/liter and under 2 mmol/liter for your LDL. Statins are useful for the treatment and prevention of atherosclerosis. Side effects can include constipation, headaches, abdominal pain, and diarrhea. Atorvastatin, fluvastatin, lovastatin, pravastatin, rosuvastatin and simvastatin are examples of statins.

Aspirin – this should not be given to patients under 16 years of age.

Drugs to lower triglyceride levels – these are fibric acid derivatives and include gemfibrozil, fenofibrate and clofibrate.

Niacin – this is a B vitamin that exists in various foods. You can only get very high doses with a doctor’s prescription. Niacin brings down both LDL and HDL levels. Side effects might include itching, headaches, hot flashes (UK: flushes), and tingling (mostly very mild if they do occur).

Anti hypertensive drugs – if you have high blood pressure your doctor may prescribe Angiotensin-converting enzyme (ACE) inhibitors, Angiotensin || receptor blockers (ARBs), Diuretics, Beta-blockers, Calcium channel blockers.
In some cases cholesterol absorption inhibitors (ezetimibe) and bile-acid sequestrants may be prescribed. They have more side effects and require considerable patient education to achieve compliance (to make sure drugs are taken according to instruction).

What Are Essential Fatty Acids?

Essential fatty acids are, as they sound, fats that are necessary within the human body. Though you’ve probably often heard the word “fats” and associated it with bad health, there are some essential fatty acids that are necessary for your survival. Without them, you could cause serious damage to different systems within the body. However, essential fatty acids are also not usually produced naturally within the body. This means that you have to obtain essential fatty acids by adding them to your diet. There are two basic types of essential fatty acids:

1. Omega-3 Essential Fatty Acids

Omega-3 essential fatty acids are necessary within the human body, but they can also be produced modestly within the body. However, you need to be sure that enough Omega-3 is in your diet. Omega-3 serves a variety of purposes within the body. First, it helps your organs to function properly and also aids in cell activity within your body. Omega-3 essential fatty acids also help cell walls to form and helps oxygen circulation throughout the body. They also work with red blood cells to make sure they are doing their job.

A lack of Omega-3 essential fatty acids could lead to blood clots, problems with memory, a decreased sense of vision, irregular heartbeat and a decrease in the functioning of your immune system. In order to be sure you’re getting enough Omega-3 essential fatty acids in your diet, try including more foods including flaxseed oil into your diet. Walnuts, sesame seeds, spinach, salmon and albacore tuna are some other foods that will help increase your Omega-3 levels.

2. Omega-6 Essential Fatty Acids

The main Omega-6 essential fatty acids that your body requires is linoleic acid. Omega-6 essential fatty acids help the body cure skin diseases, fight cancer cells and treat arthritis. However, the tricky thing with Omega-6 essential fatty acids is that most people do get enough in their diet, but they ruin it by eating foods that are high in sugar and trans fats. These factors lower the Omega-6 levels in the human body and actually do harm to you even if you are getting the right amount of Omega-6 essential fatty acids in your diet. If you’re not getting enough, though, try to include flaxseed oil, pistachios, chicken and olive oil into your diet to raise your Omega-6 levels.

Easy Ways to Get More Essential Fatty Acids into Your Diet

It’s not hard to add essential fatty acids to your current diet. All it takes is a conscious effort on your part to do it. Things like high heat temperatures can actually strip foods of their essential fatty acids. So if you’re using nuts, for example, to raise the levels of your essential fatty acids, eat them raw instead of roasting them. Check the packages of the foods you buy to see if they have high levels of essential fatty acids. Try sprinkling flaxseed oil (a great source of essential fatty acids) onto vegetables instead of using butter. These are some simple ways to deliver more essential fatty acids to your diet.

Essential Fatty Acids Keep Skin Healthy

How Essential Fatty Acids Keep Skin Healthy

Who knew that essential fatty acids and skin go hand-in-hand. Consuming fatty acids should be part of your skin care regimen, and here’s why:

What Are Essential Fatty Acids?

Essential fatty acids are some of the “good fats” that your body needs for healthy performance. ‘Essential’ designates these fatty acids as ones that are not made by the human body, and therefore must be replenished through food. These fatty acids are responsible for regulating cell function. They maintain the integrity of cellular walls, and allow transference of waste and water. This function plays a big part in skin health.

Skin Cells and Fatty Acids

Youthful skin is full of plump, water-filled cells. A skin cell’s ability to hold water decreases with age. A healthy skin cell has a healthy membrane, which keeps good things in, like water and nutrients, and allows waste products to pass out. It is a fatty acid’s job to keep that cell healthy and its membrane functioning. Not getting enough essential amino acids results in unstable membranes that cannot keep their buoyant shape, which in turn leads to saggy, aged skin.

Prevents Acne

Soft, non-oily skin is among the skin types least likely to suffer acne flare-ups. Acne occurs when glands over produce the substances keratin and sebum. They clog skin pores and result in skin infections. Essential fatty acids have a two-fold benefit for acne. First, they cause healthy cell transference, which helps dissolves the fatty deposits that block pores and cause acne. They also work to repair the skin damaged by pimples and blemishes.

Helps with Cellulite

There is no quick fix or final answer for getting rid of your cellulite. Depending on their genetics, even the thinnest of supermodels sometimes must struggle with the bumpy appearance of fat deposits pressing against the skin. However, essential fatty acids might help in the battle. There is evidence to suggest that the healthier and more supple your skin cells, the less intense the appearance of cellulite. Consuming plenty of essential fatty acids will give your skin cells more fullness and flexibility, and thereby possibly reducing the appearance of cellulite.

The Best Foods For Healthy Skin

Essential fatty acids are a must for healthy, youthful skin. Most essential fatty acids can be consumed in healthy foods. Flax seed, walnuts, salmon and canola oil, eaten in moderation, all contain enough of these fatty acids to have a positive effect on your skin. The essentials you are trying to get are omega 3 and omega 6, two of the most important components of healthy skin.

If healthy, youthful appearing skin is a priority to you, there are treatments and precautions you can take to insure your skin’s lifespan. Don’t neglect proper nutrition in the form of essential fatty acids to keep you skin cells full, flexible and strong.

Proof of how good food can be.

Red Lentil and Sweet Potato Stew

Contributed by : Daphne Oz and Mario Batali

■For Daphne’s Stew:
■Olive Oil
■1 Red Onion (finely chopped)
■Salt and Pepper to taste
■7 Carrots (thinly sliced coins)
■2 Celery Ribs (finely chopped)
■3 Garlic cloves (finely minced)
■2 cups Red Lentils (rinsed)
■2 teaspoons Cumin Seeds (toasted and ground)
■1 teaspoon Coriander (toasted and ground)
■1 teaspoon Chipotle Chili Flakes
■1/2 teaspoon Turmeric
■6 cups Water
■1 Sweet Potato (peeled and finely diced; about 1 cup)
■1 bunch Black Kale (finely shredded)
For Mario’s Croutons:

■1 cup Goat Cheese (at room temperature)
■1/3 cup Spicy Mango Chutney
■1 tablespoon Curry Powder
■Olive Oil
■1 piece of Focaccia Bread (cut into wedges)
For Daphne’s Stew: In a heavy bottomed pot over medium-high heat, add about 4 tablespoons of olive oil. Once the oil is shimmering and hot, add the onion. Season with salt and saute for 4 to 5 minutes, or until soft.

Add the carrots and celery and cook for 3 more minutes. Add the garlic and saute for 1 more minute. Add in the rinsed lentils and cook for about 2 minutes, toasting in the oil. Add the cumin seeds, coriander, chipotle chili flakes, and turmeric, and continue to toast for another minute, or until fragrant. Add the water and a big pinch of salt and pepper. Stir and bring to a boil. Reduce to a very low heat and gently simmer for about 10 minutes.

Then, carefully stir in the sweet potato and kale. Cook for another 10-15 minutes, or until the lentils are cooked through but not mushy.

For Mario’s Croutons: Preheat the oven to broil. Mix together the goat cheese, mango chutney, curry powder, and about 1 tablespoon of olive oil.

Smear the focaccia pieces with about 1 tablespoon of the goat cheese mixture and place them on a baking sheet. Put under the broiler for 1 to 2 minutes, or until the cheese is bubbly and melted.

Remove the tray from the oven and let cool slightly. Serve the croutons with the stew

Ophthalmologist

Ophthalmologist Discusses Eating Whole
Plant Foods on NBC Affiliate

In this five-minute news segment on KOBI-TV (Medford, OR), Dr. Philip Paden discusses the importance of a whole-foods, vegan diet to prevent and reverse chronic diseases. Please click here to watch the video.

Twenty Potatoes

Getting Well On Twenty Potatoes a Day

By Jeff Novick, M.S., R.D. | Posted on January 7, 2013

Chris Voigt is the executive director of the Washington State Potato Commission. In an effort to educate the public about the nutritional value of potatoes, he ate 20 potatoes a day, for 60 days straight. That’s right, his diet consisted of only potatoes and nothing else. No toppings, no chili, no sour cream, no cheese, no gravy – just potatoes and maybe some seasonings or herbs and a little oil for some of the cooking.

Watch the video about Chris Voigt’s potato diet:

Chris’s diet started on October 1, 2010 and ended November 29, 2010. His mission was to show the world that the potato is so healthy that you could live off them alone for an extended period of time without any negative impact to your health.

Of course, those of us involved in the science and practice of healthy living were curious what impact this would have on his health and well-being. We all know how potatoes have received a lot of bad press over the last few years. They’ve been said to be high in the glycemic index, will raise your blood sugar, increase your risk for diabetes, raise your triglycerides and increase your risk for heart disease and even possibly some cancers.

For the record, his goal was not to lose weight but to consume enough calories (2,200) to maintain his weight – which is the equivalent of 20 average potatoes a day.

Take a look at Chris’s numbers:

Before (9/24/2010)
Height: 6’1″
Weight: 197
BMI: 26
Cholesterol: 214 (high)
Triglycerides: 135
HDL: 45
LDL: 142 (high)
Glucose: 104 (high)
Chol/HDL ratio: 4.75
LDL/HDL ratio: 3.15

After 60 Days (11/29/2010)
Height: 6’1″
Weight: 176
BMI: 23
Cholesterol: 147
Triglycerides: 75
HDL: 48
LDL: 84
Glucose: 94
Chol/HDL ratio: 3.0
LDL/HDL ratio: 1.75

Overall Results (After 60 Days)
Weight: -21 lbs (-11%)
BMI : -3 pt
Cholesterol:-67 pts (-31%)
Triglycerides: -60 pts (-44%)
HDL: +3 pt
LDL: -58 pts (-41%)
Glucose: -10 pts (-9%)
Chol/HDL ratio:-1.75 pts (-37%)
LDL/HDL ratio: -1.40 pts (-44%)

As we can see, even though Chris was not attempting to lose weight, he did; but more importantly he had highly significant reductions in his cholesterol, triglycerides, LDL, glucose, TC/HDL ratio, LDL/HDL ratio. These numbers indicate that Chris dramatically reduced his risk for heart disease and diabetes.

The improvements were in fact greater than what we see from drugs and many intensive lifestyle programs. And he did it all in 60 days!

While I would not recommend an all potato diet for the long-term for anyone, all of this points to the simple fact that in spite of all the bad press, potatoes are a nutritious and healthy food.

Ultra-Runner

How a Plant-Based Diet Helped Make Me an Ultra-Runner

By Kathleen Leonard | Posted on January 2, 2013

I sat in my college nutrition class listening to my professor talk about nutrition. He mentioned that you could be a vegan or vegetarian and meet all your requirements to be healthy. I thought to myself, “Oh this guy is crazy! You need to eat meat, I mean, where would you get your protein from?”

I have been athletic all my life and was good at all the sports I played growing up. I maintained great fitness throughout adulthood. In 2004 I decided I wanted to run a marathon. I started running in high school and have always maintained a steady base of 3-6 miles. I figured I would read up on training for a marathon and do it right, nutrition and all.

My diet at the time consisted mainly of meat, dairy, potatoes, bread, with a little bit of fruit and vegetables. I had no problems at all with my marathon training program until I reached my higher mileage of 12+ miles. At one point I had run a few 18 milers and my body said no way. My joints were achy and it took me a week to recover just from one long run. On top of that, my immune system was crashing. I was getting sick frequently and my digestive problems seemed to get worse. I was 33 at the time and thought this should not be happening. So I backed off the running but kept my goal of running a marathon for a later date.

In the meantime, I had three young children I was raising. The colds and flus were never-ending and the diagnosis of my oldest daughter with juvenile arthritis was all I could take. I knew diet and disease were related so I decided to do some research. I learned that dairy can have horrible health effects on children. So I immediately eliminated all milk products from their diets. Once we eliminated it, my children’s health turned around. For myself, I put dairy aside too. I was stronger, less achy and soon able to run my first marathon.

Given the good results we were having sans dairy, I decided to do some research on eliminating meat. After a year, I decided that going on a plant-based diet would be a great thing to do. Shortly after all the animal-based food was gone, my health and athletic performance improved again. And in 2009 I finished my first Ironman race. I loved it so much I did it again in 2010 and finished an hour faster. On top of that I have finished numerous marathons and ultra-marathons. My recovery is faster than ever, and frequent colds are a thing of the past.

All the vitamins and minerals I get from plants aid in my recovery and keep me going strong. I have not supplemented with any protein powders of any sort and I have never felt stronger and healthier in my life. I am hoping this year will be the year I finish my first 100-mile ultra-marathon. I wish I could let my college professor know he was right.

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Ophthalmologist Discusses Eating Whole Plant Foods on NBC Affiliate

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Getting Well On Twenty Potatoes a Day

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How a Plant-Based Diet Helped Make Me an Ultra-Runner

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Ophthalmologist Discusses Eating Whole
Plant Foods on NBC Affiliate