Wednesday, March 21, 2012

The Truth About Red Meat

A recent study produced by Harvard( used to be a place for knowledge) states the dangers of eating red meat. Check out this link to see the truth:

http://www.anh-usa.org/you-are-what-your-food-ate/

Monday, March 5, 2012

The Truth About Genetic Diseases

I hear people all the time state that they have health problems because its genetic. This is a common misconception and most people do not realize that they have options. Please read the following to help bring you up to speed on how to work with your genes.

IS GENETIC MAKEUP SET IN STONE?

Dr. Joe Katzinger consults as medical researcher and health writer with SaluGenencists, Inc. He earned his ND degree from Bastyr University, and graduated summa cum laude with a bachelors of science in honor's biochemistry from Michigan State University.

ANSWER: One foundation of naturopathic medicine is the concept of personalized medicine: the matching of an individual's specific needs to the appropriate treatment. The complexity of each individual's unique biochemistry, environment, nutritional status and genetic background sometimes makes this a formidable challenge. Here, we'd like to discuss epigenetics, a relatively new but rapidly growing science which has the potential to bridge the gap between "nature and nurture," by identifying the overlap and the interactions between our genes and our environment, with the promise of tailoring treatments to a greater degree of specificity than ever before.

Epigenetics Defined

Initially coined to describe the "interaction of genes and 'other' yet unknown factors in the process of development," epigenetics is often defined as heritable changes in gene expression that are, unlike mutations, not attributable to alterations in the sequence of DNA.(1,2) In other words, although we often think of our genetic inheritance as fixed or unalterable, this is only partly true. Although the sequence of our DNA or genetic code is permanent, the programming of this code appears to be much more plastic. What is exciting is the possibility that this programming may be altered, and our basic genetic wiring is not necessarily set in stone. For example, although the code for a specific enzyme or protein is hardwired, the production of that enzyme (i.e., when it is "turned off or on") may be much more open to modification—in fact, epigenetic modifications may be the interface between our genes and our environment.

Although much of the epigenetic research done so far has concentrated on the importance of the in utero environment, intense efforts are now being focused toward modifying the epigenetic programming in adults, which was established early in life. And epigenetic modifications appear to be involved in a wide variety of illnesses, influencing susceptibility to cancer, autoimmune disease, diabetes, osteoporosis, obesity, cardiovascular disease and neurodegenerative diseases. Two of the predominant influences on the "epigenome" are nutrition, and exposure to environmental chemicals.

Nutrition and the Epigenome

Perhaps the most well-understood type of epigenetic modification is a process known as methylation. This is the addition of a chemical modifier (a methyl group) to the nucleotide bases, which comprise DNA, which essentially turns off the expression of that gene.(3) Methylation is a process, which is very much influenced by dietary factors, such as folic acid and B12. In a very dramatic example, pregnant mice prone to obesity and diabetes were supplemented with methionine, choline, folate and B12, nutrients known to be necessary for methylation. Not only did supplementation result in offspring with healthy weights, it also lowered the rates of diabetes, cancer and even changed their fur color.(4) These nutrients were shown to prevent the transgenerational amplification of obesity, which would otherwise occur over multiple generations.(5)

Transgenerational effects of diet have also been documented in humans. Investigators followed more than 200 individuals along with their parents and grandparents in northern Sweden. They documented longer survival and lower cardiovascular disease mortality if the fathers and possibly maternal grandmothers were exposed to a famine. A four-fold increase in the risk for diabetes mellitus mortality was found in children whose paternal grandfathers experienced food excess during the period just before puberty compared to those whose grandfathers experienced food scarcity.(6) This may help to explain why the increase in diabetes and obesity seems to be growing at such a rapid rate—in essence children are being programmed to be more prone to these metabolic disturbances because of the foods eaten by their parents, and this programming is amplified with each generation. But of course, that is the exciting potential of epigenetics as well. Epigenetic changes are reversible.

Several important studies have been done in monozygotic (identical) twins, which demonstrate that environmental influences do indeed modify epigenetic programming. In one of the first twin studies, the methylation patterns of 80 twins were examined. Researchers found that very young twins had nearly identical methylation patterns, but as they got older, greater differences were seen. In addition, twins that lived apart from one another also had larger differences in methylation patterns.(7) In a more recent study, nutritional and behavioral differences in twins were examined in relationship to macular degeneration. Researchers found that twins that were heavier smokers had more advanced signs of degeneration, as did those with lower intakes of vitamin D, betaine and methionine. These findings led the authors to conclude that dietary and lifestyle behaviors are responsible for the differences in macular degeneration seen between identical twins, likely due to their influences on epigenetic programming.(8) Similar findings from twins with systemic lupus erythematosus led authors to conclude that epigenetic changes may be critical to the development of autoimmune disease.(9) Interestingly, epigenetic regulation of the immune system may affect both autoimmunity and allergy, as a recent review suggests that the increase in childhood food allergies may be due to epigenetic influences.(10,11)

Environmental Chemicals and the Epigenome

In addition to dietary influences, modulation of the epigenome by exposure to environmental chemicals is gaining recognition. For example, in the same type of mice discussed above (those prone to obesity and diabetes), exposure of pregnant mice to bisphenol A (BPA, a chemical found in many plastics) was shown to change the methylation patterns of their offspring. Additionally, supplementing the mothers with folate or genistein blocked the deleterious effects of BPA.(12)

Epigenetic changes have been documented for exposure to a number of environmental chemicals, ranging from toxic metals to persistent organic pollutants to air pollution.(13) For example, lead exposure early in life changes the methylation of genes such as ß-amyloid precursor protein (APP) which persist throughout life. This is a predisposing factor for plaque development (such as seen in Alzheimer's disease) when challenged by another trigger, such as aging. The authors of this study concluded, "this model is not restricted to Pb [lead] and can be applied to nutritional deficiencies, stress, chemical exposure or any other perturbation that interferes with the epigenetic programming of gene expression."(14) A recent study of foundry workers found that exposure to air pollution caused widespread decreases in methylation, a similar finding in those with cancer and cardiovascular disease.(15-17) It appears that epigenetic programming may be an important mechanism by which environmental toxins cause disease.(18)

Conclusion

We still have a lot to learn about how epigenetic changes modify disease as well as functional outcomes, and how to induce desirable changes. We know that nutritional influences and environmental chemicals affect epigenetic programming, but that social and psychological factors also play an important role, and that the time in utero is the most critical for establishing life-long patterns.(19) It appears, however, that even adults can modify their gene expression, potentially improving overall health and reducing the risk of disease. Epigenetics holds much promise for identifying personalized therapies, which most closely address the underlying roots of both disease and health.

The research continues to grow documenting the importance of eating a nutrient dense diet and avoiding toxins—now we know this affects our health not only through biochemistry, but also through genetic activation/deactivation that can affect our progeny through generations. Epigenetics reminds us of the work of Hahnemann, who two centuries ago observed transgenerational effects caused by poor lifestyle choices (which he called miasms). His ideas were ridiculed at the time, but research is showing that this pioneer was insightful indeed.

References:

1. Szyf M. The implications of DNA methylation for toxicology: toward toxicomethylomics, the toxicology of DNA methylation. Toxicol Sci. 2011 Apr;120(2):235-55.
2. Hamilton JP. Epigenetics: principles and practice. Dig Dis. 2011;29(2):130-5.
3. McGowan PO, et al. Diet and the epigenetic (re)programming of phenotypic differences in behavior. Brain Res. 2008 Oct 27;1237:12-24.
4. Cooney CA, et al. Maternal methyl supplements in mice affect epigenetic variation and DNA methylation of offspring. J Nutr. 2002;132(8 Suppl):2393-2400S
5. Waterland RA, et al. Methyl donor supplementation prevents transgenerational amplification of obesity. Int J Obes (Lond). 2008 Sep;32(9):1373-9.
6. Kaati G, Bygren LO, Edvinsson S. Cardiovascular and diabetes mortality determined by nutrition during parents' and grandparents' slow growth period. Eur J Hum Genet. 2002 Nov;10(11):682-8.
7. Fraga MF, et al. Epigenetic differences arise during the lifetime of monozygotic twins. Proc Natl Acad Sci U S A. 2005 Jul 26;102(30):10604-9.
8. Seddon JM, et al. Smoking, dietary betaine, methionine, and vitamin d in monozygotic twins with discordant macular degeneration: epigenetic implications. Ophthalmology. 2011 Jul;118(7):1386-94.
9. Javierre BM, et al. Changes in the pattern of DNA methylation associate with twin discordance in systemic lupus erythematosus. Genome Res. 2010 Feb;20(2):170-9.
10. Janson PC, et al. Epigenetics - the key to understand immune responses in health and disease. Am J Reprod Immunol. 2011 Jul;66 Suppl 1:72-4
11. Tan TH, et al. The role of genetics and environment in the rise of childhood food allergy. Clin Exp Allergy. 2011 Jul 19. doi: 10.1111/j.1365-2222.2011.03823.x. [Epub ahead of print]
12. Dolinoy DC, et al. Maternal nutrient supplementation counteracts bisphenol A-induced DNA hypomethylation in early development. Proc Natl Acad Sci U S A. 2007 Aug 7;104(32):13056-61.
13. Baccarelli A, Bollati V. Epigenetics and environmental chemicals. Curr Opin Pediatr. 2009 Apr;21(2):243-51.
14. Zawia NH, Lahiri DK, Cardozo-Pelaez F. Epigenetics, oxidative stress, and Alzheimer disease. Free Radic Biol Med. 2009 May 1;46(9):1241-9.
15. Tarantini L, et al. Effects of particulate matter on genomic DNA methylation content and iNOS promoter methylation. Environ Health Perspect. 2009 Feb;117(2):217-22.
16. Kulis M, Esteller M. DNA methylation and cancer. Adv Genet. 2010;70:27-56.
17. Castro R, et al. Increased homocysteine and Sadenosylhomocysteine concentrations and DNA hypomethylation in vascular disease. Clin Chem. 2003 Aug;49(8):1292-6.
18. Bollati V, Baccarelli A. Environmental epigenetics. Heredity. 2010 Jul;105(1):105-12.
19. Szyf M, et al. Maternal care, the epigenome and phenotypic differences in behavior. Reprod Toxicol. 2007 Jul;24(1):9-19.