Egg whites are. Egg yolks are not. Though eggs are packed with protein and nutrients, eggyolks are also packed with cholesterol, which can harm our hearts. Comment” The egg white is pure animal protein and should also be avoided.” 

To help unscramble the truth, let’s talk a bit more about cholesterol.

When we hear the word “cholesterol,” it usually refers to one of two things. There is dietary cholesterol, which is the cholesterol we eat. Egg yolks have the most dietary cholesterol of any food. With just one yolk, we’re swallowing about 200 milligrams of dietary cholesterol. That’s the amount the American Heart Association recommends most of us not exceed for the entire day. For optimal prevention against heart disease, the Pritikin Eating Plan recommends no more than 100 milligrams of dietary cholesterol a day.

Counsels Dr. Kenney: “If you eliminate three egg yolks a day, you will likely lower your blood cholesterol at least 15%, on average, and improve the overall health of your arteries.”

Blood, or serum, cholesterol is the amount of cholesterol in our blood. About 85% of the cholesterol in our blood comes from our liver. And here’s a really important point: Our liver manufactures all the cholesterol our bodies need.

About 15% of the cholesterol in our blood comes from the food we eat – yes, dietary cholesterol. Consistently, research has found that the more dietarycholesterol we eat, the higher our blood cholesterol levels rise, and the greater our risk of heart disease. That’s why it’s so important to keep a lid on the amount of cholesterol we eat.

Saturated and Trans Fats

Now, it’s certainly true that dietary cholesterol is not the only thing that raises blood cholesterol. Saturated and trans fats are spectacularly good at ratcheting up blood cholesterol levels. We get saturated and trans fat from foods like red meat, cheese, and butter, as well as from processed foods, everything from margarine to frozen entrees, that contain ingredients like coconut oil, palm oil, and partially hydrogenated oils.

Let’s get back to dietary cholesterol. For decades, scientific research has demonstrated that rising intake of egg yolks, rich in dietary cholesterol, contributes to rising blood cholesterol levels.

Here is just a sampling of that research…

Just One Extra Egg a Day

As early as 1984, in a well-designed clinical study published in the leading medical journal The Lancet¹, researchers from Harvard Medical School studied the effects of adding just one extra-large egg a day to the regular diets of young, healthy men and women. All of them were lacto-vegetarians (vegetarians who also ate dairy products).

That one daily jumbo egg increased the subjects’ dietary cholesterol intake on average from 97 to 418 milligrams per day. After three weeks – just three weeks – blood cholesterol levels among the men and women had also shot up. Levels of LDL (bad) cholesterol rose on average 12%. “Ingestion of egg seems selectively to raise cholesterol and protein in LDL particles in the plasma of free-living normal people,” lead author Frank M. Sacks, MD, and colleagues concluded.

Egg Whites vs Whole Eggs

In another study², a carefully controlled clinical trial published in 2006, researchers at the University of Sao Paulo in Brazil fed three egg whites daily to one group of healthy young men, and three whole eggs daily to another group of men, also young and healthy. The study lasted 15 days. Except for the egg variations, all the men were eating the exact same thing. Their meals, prepared daily by the university, were heart-healthy-style – fairly low in fat and high in a variety of whole foods like fruits, green vegetables, beans, chicken, and fish.

Among the men in the group eating three egg whites daily, total intake of dietary cholesterol averaged only 174 milligrams per day. Among the men eating three whole eggs a day (egg whites plus egg yolks) daily dietary cholesterol intake averaged a whopping 804 milligrams.

More Eggs, Higher LDL

Along with increased dietary cholesterol, the egg yolk eaters ended up with increased blood cholesterol. Their LDL bad cholesterol, after 15 days of eating whole eggs, was about 30% higher compared to the egg white eaters. “A high-cholesterol diet clearly enhances LDL levels,” wrote the authors. At the end of the study, the egg white eaters had average LDL levels of 86. The LDL levels of the whole egg eaters was 120.

Chylomicrons

There was more troubling news. The scientists found that in addition to raising LDL cholesterol, the three-whole-eggs-a-day diet hindered the body’s ability to clear out artery-clogging chylomicron remnants. Chylomicrons are particles, like LDL, that transport triglycerides and other fats to various cells throughout the body. Chylomicronsalso absorb the dietary cholesterol we eat. Once chylomicrons start “unloading” their cargo, they become chylomicron remnants, which are taken up by the liver and discarded from the body. But if these chylomicrons remnants are stuffed with dietary cholesterol and fats, they tend to “hang around” in our bodies longer, taking up residence in our artery walls, just as LDL cholesterol does, where they can wreak havoc.

And sure enough, the Brazilian study found that eating three egg yolks daily “increased the residence time of chylomicron remnants, which may have undesirable effects related to the development of coronary artery disease,” the scientists wrote.

Fouling Up HDL

“The cholesterol from these chylomicron remnants can also be passed to HDL particles, and that’s potentially a big problem,” points out Dr. Jay Kenney, Nutrition Research Specialist at the Pritikin Longevity Center. “It can contribute to the conversion of HDL from ‘good’ to ‘bad’ cholesterol, from being anti-inflammatory to pro-inflammatory. And no longer is HDL doing its job of transporting cholesterol out of the artery walls and back to the liver for disposal.”

“Unfortunately,” continues Dr. Kenney, “many physicians don’t pay attention to chylomicrons, and ignore their role in promoting coronary artery disease, or atherosclerosis. That’s troubling, especially since doctors’ key strategy for fighting heart disease – prescribing statins – does little to reduce the formation of chylomicrons or the amount of chylomicron remnants burrowing into the artery wall and damaging arteries.”

The good news is that an optimal heart-health food and fitness plan like the Pritikin Program does appear to reduce chylomicron activity, “which may help explain why lifestyle programs like Pritikin can reverse atherosclerosis better than statins,” notes Dr. Kenney.

New Research

The most recent study³ documenting the dangers of egg yolks was published this month by scientists at the Stroke Prevention & Atherosclerosis Research Centre in Ontario, Canada. The researchers looked at more than 1,200 people, average age 61, who already had artery disease, asking them about their daily diets and any other cardiovascular risk factors they might have, including smoking. Then, using carotid ultrasound imaging, the researchers found that those people who ate the most whole eggs had the most plaque-ridden arteries.

The scientists also noted that the people who had eaten the most eggs over the years had even more plaque build-up than those with the highest cholesterol levels or body weights.

The egg industry must have been concerned about consumer reaction to this new study because immediately after its online publication, doctors affiliated with the industry shot out press statements criticizing the study, pointing out, for example, that the subjects with the higher egg intakes also tended to be heavy smokers.

“Nice spin,” smiles Dr. Kenney, “but these press statements failed to mention that the Canadian scientists had in fact looked for a statistically significant correlation between egg yolk consumption and smoking history. They found none.”

Bottom Line:

Counsels Dr. Kenney: “If you eliminate three egg yolks a day, which is about 600 milligrams of dietary cholesterol, you will likely lower your blood cholesterol at least 15%, on average, and improve the overall health of your arteries. That’s very good news for your heart.”

Do enjoy egg whites. Breakfast at the Pritikin Longevity Center includes a big, beautiful egg-white-omelet bar full of fresh, colorful additions like salsa, green onions, nonfat ricotta cheese, and roasted red peppers.

But steer clear of egg yolks most of the time, if not all. What the egg industry describes as “nature’s perfect food” is not perfect for your arteries.

What is perfect is a lifestyle program like Pritikin that substantially limits saturated and trans fats as well as dietary cholesterol, and promotes an eating plan full of whole, fiber-rich foods, plus daily exercise.

Atkins “Nightmare” Diet

When Dr. Atkins Diet Revolution was first published, the President of the American College of Nutrition said, “Of all the bizarre diets that have been proposed in the last 50 years, this is the most dangerous to the public if followed for any length of time.”[1]

When the chief health officer for the State of Maryland,[2] was asked “What’s wrong with the Atkins Diet?” He replied “What’s wrong with… taking an overdose of sleeping pills? You are placing your body in jeopardy.” He continued “Although you can lose weight on these nutritionally unsound diets, you do so at the risk of your health and even your life.”[3]

The Chair of Harvard’s nutrition department went on record before a 1973 U.S. Senate Select Committee investigating fad diets: “The Atkins Diet is nonsense… Any book that recommends unlimited amounts of meat, butter, and eggs, as this one does, in my opinion is dangerous. The author who makes the suggestion is guilty of malpractice.”[4]

The Chair of the American Medical Association’s Council on Food and Nutrition testified before the Senate Subcommittee as to why the AMA felt they had to formally publish an official condemnation of the Atkins Diet: “A careful scientific appraisal was carried out by several council and staff members, aided by outside consultants. It became apparent that the [Atkins] diet as recommended poses a serious threat to health.”[5]

The warnings from medical authorities continue to this day. “People need to wake up to the reality,” former U.S. Surgeon General C. Everett Koop writes, that the Atkins Diet is “unhealthy and can be dangerous.”[6]

The world’s largest organization of food and nutrition professionals,[7] calls the Atkins Diet “a nightmare of a diet.”[8] The official spokesperson of the American Dietetic Association elaborated: “The Atkins Diet and its ilk–any eating regimen that encourages gorging on bacon, cream and butter while shunning apples, all in the name of weight loss–are a dietitian’s nightmare.”[9] The ADA has been warning Americans about the potential hazards of the Atkins Diet for almost 30 years now.[10] Atkins dismissed such criticism as “dietician talk”.[11] “My English sheepdog,” Atkins once said, “will figure out nutrition before the dieticians do.”[12]

The problem for Atkins (and his sheepdog), though, is that the National Academy of Sciences, the most prestigious scientific body in the United States, agrees with the AMA and the ADA in opposing the Atkins Diet.[13] So does the American Cancer Society;[14] and the American Heart Association;[15] and the Cleveland Clinic;[16] and Johns Hopkins;[17] and the American Kidney Fund;[18] and the American College of Sports Medicine;[19] and the National Institutes of Health.[20]

In fact there does not seem to be a single major governmental or nonprofit medical, nutrition, or science-based organization in the world that supports the Atkins Diet.[21] As a 2004 medical journal review concluded, the Atkins Diet “runs counter to all the current evidence-based dietary recommendations.”[22]

A 2003 review of Atkins “theories” in the Journal of the American College of Nutrition concluded: “When properly evaluated, the theories and arguments of popular low carbohydrate diet books… rely on poorly controlled, non-peer-reviewed studies, anecdotes and non-science rhetoric. This review illustrates the complexity of nutrition misinformation perpetrated by some popular press diet books. A closer look at the science behind the claims made for [these books] reveals nothing more than a modern twist on an antique food fad.”[23]

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.

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).