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A. H Bittles has written:

'The application of tissue culture techniques to the study of inborn errors of metabolism, with particular reference to cystathionine synthese deficiency'

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A. H Bittles has written:

'The application of tissue culture techniques to the study of inborn errors of metabolism, with particular reference to cystathionine synthese deficiency'

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Plant protein is healthier and more humane.

Animal protein contains carnitine, which is not an essential amino acid for humans. Your intestinal bacteria feed on the carnitine in animal protein and produce trimethylamine-N-oxide (TMAO). TMAO promotes the growth of fatty deposits on the walls of your arteries and and slows the removal of cholesterol from the arteries' walls.

Animal proteins contain very large amounts of sulfur, especially in the essential amino acid methionine and the conditionally essential amino acid cysteine. Your body makes other sulfur-containing amino acids out of these, including keto-methionine, cystine, homocysteine, cystathionine, taurine, and cysteic acid.

Even though you need a small amount of sulfur-containing amino acids, an excess of these amino acids beyond your needs causes the following problems:

  1. Your body breaks down the sulfur-containing amino acids into powerful sulfuric acid. Excess acid causes your body to use calcium from your bones to maintain pH. This can lead to osteoporosis and kidney stones.
  2. Your body breaks down methionine (which is very high in animal protein) into homocysteine, which is a risk factor for heart attacks, strokes, closure of your leg arteries (peripheral vascular disease), blood clots in your legs (venous thrombosis), cognitive impairment, dementia, Alzheimer's disease, and depression.
  3. Methionine feeds cancerous tumors. Normal cells can get the sulfur they need from other sulfur-containing amino acids, but cancer cells, including breast, lung, colon, kidney, melanoma, and brain cancers, need methionine. Meat and dairy products also raise the levels of a powerful growth-stimulating hormone, called insulin-like growth factor-1 (IGF-1), which magnifies the effects of methionine to promote cancer, including cancers of the breast, colon, prostate, and lung.
  4. Sulfur from high-methionine (animal) protein is toxic to the tissues of your intestine, and can damage your colon, leading to a disease called ulcerative colitis.

Casein, the main protein in dairy foods, incites cancer progression.

The absence of casein and the lower amounts of carnitine, methioine, and cysteine in plant protein have several advantages:

  1. Plant proteins do not incite cancer progression.
  2. A diet based on plant food is low in carnitine, which keeps your arteries healthy.
  3. Plant-based diets are low in both calories and methionine. Low-calorie diets slow the aging process and prolong life. Low-methionine diets also prolong life.
  4. Plant protein makes you smell better. The high sulfur in animal protein causes bad breath, body odor, and flatulence that smells like rotten eggs.
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(Taken from Chapter 8: Feeding Beef Cattle, p. 273 of Beef Cattle Science by M.E. Ensminger and R.C. Perry):

Sulfur is one macromineral that is important for the health of cattle. Macrominerals include, besides Sulfur, Calcium, Phosphorus, Salt (NaCl), Magnesium, and Potassium. Sulfur is a component of protein, some vitamins, and several important hormones. The common sulfur-containing amino acids are methionine, cysteine, and cystine. Also, the following amino acid derivatives contain sulphur: cystathionine, taurine, and cysteic acid. Methionine is a key amino acid because all other sulfur compounds, except B-vitamins thiamin and biotin, can be synthesized from methionine.

All feeds contain some sulfur, but the amount usually depends on the protein content of the feed--generally speaking, the higher the protein count, the higher the sulfur content. Availability of the sulfur in the feed to microbial reduction in the rumen may be as much of a concern as the actual amount that is present.

(From Table 8-5 of Beef Cattle Science, Chapter 8, p. 274-5):

Body functions that involve sulfur include protein synthesis and metabolism, fat and carbohydrate metabolism, blood clotting, endocrine function, and intra- and extra-cellular fluid acid-base balance. Sulfur has both structural and metabolic functions; it is found in virtually every tissue and organ of the body. Muscle has a fairly constant nitrogen to sulfur ratio of 15:3:1. The total body content of sulfur is approximately 0.15%.

Deficiency of sulfur include such symptoms as depressed appetite, weight loss, weakness, excessive salivation, watery eyes, dullness, emaciation, and death. A lack of sulfur also results in a microbial population that does not utilize lactate. Usually deficiencies of sulfur are reported in cattle that are fed high-grain rations and supplemented with non-protein nitrogen.

Toxicity level of sulfur, according to the NRC (Nutritional Research Center) is 0.40% of the ration dry matter. Sulfur toxicity is characterized by restlessness, diarrhea, muscular twitching, dyspnea, and in prolonged cases of inactivity followed by death.

A ration (dry matter) should have a sulfur level of a minimum of 0.15% and a maximum of 0.4%. If the ration is higher or lower than these numbers, toxicity or deficiency levels will develop, respectively.

Some practical sources of this mineral include feeds that are high in protein (these usually high in sulfur as well). The microbial population of the rumen has the ability to convert inorganic sulfur into organic sulfuric compounds that can be used by the animal. So, either organic or inorganic sulfur can be used by cattle. Most feedstuffs provided to beef cattle contain sufficient sulfur to meet their needs.

Note that copper requirements are increased by both sulfur and molybdenum. Selenium can also be a replacement for sulfur in some organic compounds.

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There was no one person who is credited with having discovered the theory that milk helps bones get stronger. Early studies linked calcium with stronger bones, and milk is a rich source of calcium.

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Definition

Homocystinuria is an inherited disorder that affects the metabolism of the amino acidmethionine.

Alternative Names

Cystathionine beta synthase deficiency

Causes, incidence, and risk factors

Homocystinuria is inherited in families as an autosomal recessive trait. This means that the child must inherit the non-working gene from both parents to be seriously affected.

Homocystinuria has several features in common with Marfan syndrome. Unlike Marfan syndrome, in which the joints tend to be "loose," in homocystinuria the joints tend to be "tight."

Symptoms

Newborn infants appear healthy. Early symptoms, if present at all, are not obvious.

Symptoms may occur as mildly delayed development or failure to thrive. Increasing visual problems may lead to diagnosis of this condition.

Other symptoms include:

Signs and tests

While performing a physical examination on the child, the health care provider may notice a tall, thin (Marfanoid) stature.

Other signs include:

  • Curved spine (scoliosis)
  • Deformity of the chest
  • Dislocated lens of the eye

If there is poor or double vision, an ophthalmologist should perform a dilated eye exam to look for dislocation of the lens or nearsightedness.

There may be a history of frequent blood clots. Mental retardation, slightly low IQ, or psychiatric disease are common.

Tests:

Treatment

There is no cure for homocystinuria. However, many people respond to high doses of vitamin B6 (also known as pyridoxine). Slightly less than half of patients respond to this treatment.

Those who do respond will need to take vitamin B6 supplements for the rest of their lives. Those who do not respond need to eat a low-methionine diet. Most will need treatment with trimethylglycine (a medication also known as betaine).

Neither a low-methionine diet nor medication will improve existing mental retardation. Medication and diet should be closely supervised by a physician with experience treating homocystinuria.

A normal dose folic acid supplement and added cysteine (an amino acid) in the diet are helpful.

Expectations (prognosis)

Although no cure exists for homocystinuria, vitamin B6 therapy can help about half of people affected by the condition.

If the diagnosis is made while a patient is young, starting a low methionine diet quickly can prevent some mental retardation and other complications of the disease. For this reason, some states screen for homocystinuria in all newborns.

Patients with persistent rises in blood homocysteine levels are at increased risk for blood clots. Clots can cause significant medical problems and shorten lifespan.

Complications

Most serious complications result from blood clots. These episodes can be life threatening.

Dislocated lenses of the eyes can severely impair vision. Lens replacement surgery should be considered.

Mental retardation is a serious consequence of the disease. However, it can be lessened if diagnosed early.

Calling your health care provider

Call your health care provider if you or a family member shows symptoms of this disorder, particularly if there is a family history of homocystinuria. Also call if you have a family history and are planning to have children.

Prevention

Genetic counseling is recommended for prospective parents with a family history of homocystinuria. Intrauterine diagnosis of homocystinuria is available. This involves culturing amniotic cells or chorionic villi to test for cystathionine synthase (the enzyme that is missing in homocystinuria).

If there are known specific genetic mutations in the parents or family, samples from chorionic villus samplingor amniocentesiscan be used to test for these mutations.

References

Rezvani I. Defects in metabolism of amino acids. In: Kliegman RM, Behrman RE, Jenson HB, Stanton BF. Nelson Textbook of Pediatrics. 18th ed. Philadelphia, Pa: Saunders Elsevier; 2007:chap 85.

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