Mark Hyman, M.D.
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 Maximize Methylation
A key objective in correcting malnutrition is maximizing methylation. methylation is a crucial step for our bodies in the process of repairing our DNA, controlling which of our genes are turned on or off, and producing proteins.
Here's how to maximize methylation:
• Monitor and maintain your blood homocysteine level—this should be between 5 and 9.
• Minimize animal protein, sugar, and saturated fat. |
Dr. Steve Blake
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 Folate also assists with methylation by increasing the SAMe in the cell.
Cancer is thought to arise from excess expression of certain genes within DNA. methylation quiets RNA replication and can help the cells regulate excess growth. Folate may be helpful in preventing breast cancer in women who drink alcohol. Sufficient folate intake has also been associated with lower colorectal cancer risk.
FOLATE AND VITAMIN B12
High levels of folic acid supplementation, especially above 1000 meg daily, can mask symptoms of vitamin B12 deficiency. |
Bill Sardi
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 Journal Virology 73: 9959-68, 1999] A process called methylation can inhibit genes that trigger latent viruses from becoming active. Folic acid is involved in methylation. A shortage of folic acid can facilitate the activation of cancer-causing viruses like Epstein-Barr.
Since Epstein-Barr virus is transmitted through saliva, it often infects the oral cavity. It can travel to the gastric tract and cause infection there. Viruses remain dormant, hiding in nervous tissue from the immune system. Years later they can erupt. |
Dr. Steve Blake
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| Betaine supplies methyl groups for various methylation reactions. One of these methylation reactions results in the conversion of homocysteine to methionine.
No RDA has been set for choline, but the adequate daily intake (AI) has been set at 550 mg for men and 425 mg for women. Average dietary intake is thought to be adequate. Healthy food sources include Brussels sprouts, broccoli, peanut butter, and salmon.
Choline supplements are available as choline chloride and choline bitartrate. Lecithin is a good source of choline and contains 13 percent choline. |
Bill Sardi
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| Cancer Research 64: 8788-93, 2004]
Researchers are attempting to temporarily use methylation inhibitors to uncloak hidden Epstein-Barr in tumor cells. Countering methylation will, however, raise homocysteine levels, which is also problematic. A class of drugs known as histone deacetylase inhibitors could potentially be used to treat Epstein-Barr related tumors by de-methylating tumor cells only, not healthy cells, which would render them more susceptible to the immune system. |
Mark Hyman, M.D.
See book keywords and concepts |
| Maximize Methylation
A key objective in correcting malnutrition is maximizing methylation. methylation is a crucial step for our bodies in the process of repairing our DNA, controlling which of our genes are turned on or off, and producing proteins.
Here's how to maximize methylation:
• Monitor and maintain your blood homocysteine level—this should be between 5 and 9.
• Minimize animal protein, sugar, and saturated fat. |
by Michael Murray, N.D. and Joseph Pizzorno, N.D.
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| It functions closely with folic acid and vitamin B12 in "methylation" reactions. methylation is the process of adding a single carbon unit (a methyl group) to another molecule. SAMe is many times more effective in transferring methyl groups than other methyl donors. methylation reactions are critical in the manufacture of many body components, especially brain chemicals, as well as in detoxification reactions. |
Stephen T. Sinatra, M.D.
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 L-carnitine synthesis begins with the methylation of the amino acid L-lysine by S-adenosyl-L-methio-nine (SAM).
After several more complex steps requiring consecutive methylations and the interaction of several enzymes—and the vitamins and minerals I described—carnitine is made in the body. However, it is important to note that dietary deficiencies of L-lysine or in any of the vitamins and minerals mentioned will result in inadequate synthesis of L-carnitine. This is why dietary deficiencies of L-carnitine and/or the cofactors for its biosynthesis are extremely important. |
Jonny Bowden, Ph.D., C.N.S.
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 The health of all those "systems" depends heavily on a well-oiled system of methylation.
SAMe is arguably the most effective "natural" antidepressant around. And one of the best things about it is that you'll know whether it's working within a week. (Actually this is true for the majority of people, but in some less common cases it may take up to five weeks to work, about the same as a pharmaceutical antidepressant in the SSRI class, which includes Prozac, Paxil, and Zoloft. |
Dr. Sharon Moalem
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 The choline triggered a methylation pattern that turned off the gene that normally acted to limit cell division in the memory center of the brain. With the cell division governor turned off, these mice started producing memory cells in high gear—and sure enough, they developed mighty mouse memories. Their neurons fired more rapidly and could fire more often. As adults, these megabrain mice broke all the records in all the mazes. |
| The exact same set of genes can produce different outcomes depending on which genes have undergone methylation and which have not. There was a whole new layer to consider—a set of reactions that acted outside and above the genetic code, changing its result without changing the code itself. (That outside and above is where epigenetics gets its name— from the Greek prefix epi, meaning upon, after, or in addition. |
Mehmet C. Oz., M.D. and Michael F. Roizen, M.D.
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 That blood pulsates into the aorta—the body's
Your Oww Meth Lab
A process in your body called methylation may sound like it's illegal in forty-nine states, but it's one that your body depends on. The process-changing a molecule by adding a methyl group-helps detox your body, repair DNA, and form new cells. As you age, the reduced ability to methylate is associated with heart disease as well as Alzheimer's and diabetes. What can you do? Make sure you're getting cofactors for methyl transfer like those found in fish and whole grains. |
| Also, taking B12 and folic acid (see chart on page 357 for doses) seems to help methylation by reducing levels of homocysteine. largest artery—which delivers oxygen-rich blood to the rest of the body as well as to the coronary arteries surrounding the heart.
Much of heart disease happens in your arteries—the tunnels that feed both nutrients and toxins to all your organs—rather than in your heart itself. |
Jonny Bowden, Ph.D., C.N.S.
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| The researchers theorized that the deficiency probably caused impaired central nervous system reactions (specifically a chemical reaction called methylation, impairment of which is a characteristic feature of Alzheimer's). They also believe that there might be a genetic predisposition to Alzheimer's, and that some individuals are actually born unable to properly absorb B12.
Keep in mind that supplementation results in less improvement for those who have had fullblown Alzheimer's symptoms for more than six months. |
| SAMe works best with adequate B vitamins, especially folate, B6, and B12, which also support the methylation process in the brain and elsewhere.
Natural Prescription for SAMe
Doses and Precautions
SAMe has been used in doses ranging from 200-1,600 mg a day.
A common dose for depression is 800 mg a day, though people take up to 1,600 mg.
For liver problems, up to 1,600 mg a day.
For bone and joint health, the typical dose is between 200 and 1,200 mg a day.
SAMe is usually taken in divided doses. |
| And remember methylation (see page 309)? SAMe's outstanding properties as a methylating agent help keep liver membranes fluid. Anyone with liver disease or problems, such as hepatitis, should consider SAMe as an adjunct to treatment.
It's also been shown in research to significantly prevent or reverse the toxicity that can be induced in the laboratory by drugs, alcohol, or chemicals. |
| When methylation is compromised it's like having sticky, sludgy spark plugs. Everything slows down, energy is compromised, and things just don't work right.
Enter SAMe. SAMe is the ultimate "methyl donor." That means it literally donates a methyl group wherever it's needed, keeping the relay races running smoothly. It virtually passes a torch to whoever needs it so that the race never has to slow down or get derailed while someone goes looking for a torch. |
| And the secret to its effectiveness for so many disparate conditions is a process in the body called methylation.
Think back to your high school track meets and remember what it was like to watch a relay race. Remember how the stick was passed from
SAMe
EPRESSION, ARTHRITIS, liver disease, and fibromyalgia. What could these four completely distinct conditions possibly have
11^*1 C3 f*n l**T*^ ft * %m-J I N/'d- LI |I?» / * 11 * C!5 ILI \* ^3 I'll 13 cLtC^ Cj with a wonderful compound called SAMe. runner to runner? |
Dr. Steve Blake
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| Cancer is thought to arise from excess expression of certain genes within DNA. methylation quiets RNA replication and can help the cells regulate excess growth. Folate may be helpful in preventing breast cancer in women who drink alcohol. Sufficient folate intake has also been associated with lower colorectal cancer risk.
FOLATE AND VITAMIN B12
High levels of folic acid supplementation, especially above 1000 meg daily, can mask symptoms of vitamin B12 deficiency. |
Dr. Sharon Moalem
See book keywords and concepts |
| These drugs were all but spray painting the genome with new methylation patterns, turning off as many genes as they were turning on— hundreds of each.
Don't get me wrong—epigenetics has unbelievable potential to have a positive impact on human health. A Rutgers University professor named Ming Zhu Fang has studied the effect of green tea on human cell lines. He's found that compounds in green tea inhibit the placement of methyl markers on genes that help to fight colon, prostate, and esophageal cancer. |
| Azacitidine inhibits the methylation of certain genes in blood cells, helping to restore proper DNA function and reducing the risk that MDS will develop into leukemia. Azacitidine was met with tremendous excitement at its introduction. Peter Jones, a professor of biochemistry and molecular biology at the University of Southern California, said:
This is the first approved drug in a new kind of therapy— epigenetic therapy. That gives it tremendous potential importance not just in this disease, but in a host of others as well.
Of course, in a report by Dr. |
Thomson Healthcare, Inc.
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 Melikian V, Paton A, Leeming RJ et al: Site of reduction and methylation of folic acid in man. Lancet; 2(7731):955-957. 1971
Milunsky A, Jick H, Jick SS et al: Multivitamin/folic acid supplementation in early pregnancy reduces the prevalence of neural tube defects. JAMA; 262(20):2847-2852. 1989
Morita H, Tagushi J, Kurihara H et al: Genetic polymorphism of 5, 10-methylenetetrahydrofolate reductase (MTHFR) as a risk factor for coronary artery disease. Circulation; 95(8):2032-2036. 1997
Morgan SL, Oster RA, Lee JY et al. |
Dr. Sharon Moalem
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| Now we're starting to see drugs actually designed to affect methylation patterns. The first of these drugs was approved by the Food and Drug Administration in 2004. Called azacitidine in its generic form, it was hailed as a breakthrough for the treatment of myelodysplas-tic syndrome, or MDS. MDS is a collection of blood disorders that is very difficult to treat and often leads to potentially deadly leukemia—a new drug for MDS would be a significant advance. |
Thomson Healthcare, Inc.
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| Antidepressant Effects: A low level of SAMe in the cerebrospinal fluid (CSF) of some depressed patients suggests a possible disorder of methylation in the central nervous system and provides a rational basis for using SAMe therapeutically (Bottiglieri et al, 1994, 1990). Parenterally administered SAMe crosses the blood-brain barrier and, when present in high levels in the CSF, increases the CSF concentrations of 5-hydroxyindoleacetic acid and homovanillic acid while reducing serum prolactin levels, reflecting increased turnover of serotonin and dopamine. |
Erich Grotewold
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 There are six major anthocyanidins acting as central chromophores of anthocyanins: pelargonidin, cyanidin, peonidin, delphinidin, petunidin, and malvidin, which differ only in the extent of B-ring hydroxylation and methylation (Figure 6.4). In general, pigments of pelargonidin and cyanidin derivatives produce red and purple color, respectively, whereas those of delphinidin show purple or blue color (Goto and Kondo, 1991). |
| DNA methylation and transgene silencing in Petunia hybrida, Curr Top Microbiol
Immunol 197: 15-28.
Mo, Y., Nagel, C. and Taylor, L. P., 1992, Biochemical complementation of chalcone synthase mutants defines a role for flavonols in functional pollen, Proc Natl Acad Sci USA 89: 7213-7217.
Mol, J., Grotewold, E. and Koes, R., 1998, How genes paint flowers and seeds, Trends Plant Sci 3: 212-217.
Moreno, M. A, Chen, J., Greenblatt, I. and Dellaporta, S. L., 1992, Reconstitutional mutagenesis of the maize P gene by short-range Ac transpositions, Genetics 131: 939-956.
Morita, Y., Hoshino, A. |
| DFR-B gene, and the integrated transposon appears to affect DNA methylation of a particular site within the DFR-B promoter (Iida et al., 2004; J.D. Choi and A. Hoshino, unpublished). Thus, the genetic change caused by the transposon integration results in a situation in which the epigenetic gene regulation can play important roles in flower pigmentation (Iida et al., 2004). It is likely that both genetic and epigenetic regulation associated with transposons can cooperatively act on the generation of flower pigmentation patterns.
4.3.2. |
| The flower variegation was caused by transcriptional gene silencing (TGS) due to DNA methylation of the promoter of the DFR transgene (Meyer, 1995). Subsequently, posttranscriptional gene silencing (PTGS) of transgenes and endogenous genes were reported in the petunia CHS and DFR genes (Napoli et al., 1990; van der Krol et al., 1990). |
| The extent of hydroxylation and methylation of the B-ring, indicated by B, determine the six major anthocyanins.
Blue and reddish flowers of the morning glories /. nil and I. tricolor (Figure 6.3) contain peonidin-3-O-sophoroside and pelargonidin-3-O-sophoroside derivatives with four additional glucose residues and three caffeoyl moieties, which are called Heavenly Blue Anthocyanin (HBA) and Wedding Bell Anthocyanins (WBA), respectively. The latter was found in the magenta or fuchsia mutants (Table 6.1) (Goto and Kondo, 1991; Hoshino et al., 2003). |
| On the other hand, some rearrangements may take place during the methylation of flavonoid -OH groups, and additional compounds become present in the reaction mixture after the derivatization. This is especially the case for flavanones, which rearrange to chalcones. However, mass spectra of methylated flavonols, flavones, or isoflavones give good structural information about the corresponding isomers. The comparison of mass spectra of silylated and methylated isoflavones from extracts obtained from lupine roots was previously demonstrated (Stobiecki and Wojtaszek, 1990). |
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