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HUMAN DEFECTS

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                         THE HUMAN DEFECTS

THE HUMAN DEFECT  # 1 Unable to manufacturing Vitamin C (ascorbate) by our own body.

About 40 million years ago our ancestor lost ability for endogenous ascobate production this was the result of a mutation of the gene encoding for the enzymes L-GLULONO-G-LACTONE OXIDASE (GLO), a key enzyme in the conversion of glucose to ascorbate. As a result of this mutation all descendants became dependent on dietary ascorbate  intake. The species that lack of this enzymes are  (1) humans, (2) gorillas, (3) guinea pigs and (4) fruit bats.

As you know, lack of vitamin C cause scurvy. However according to Mattias Rath, M.D. and Linus Pauling Ph D.’s study. Why animals that make their own vitamin C up to 20 gm. per day have no heart attack in spite of high cholesterol over 500 mg/ml in some species.

According to their study all species that lack of endogenous ascorbate production have high blood lipoprotein called Lp(a). As you might recall from previous subject on this website related to human evolution. The origin of all Homo sapiens sapiens came from tropical area in Africa, which had plenty of fruits and fresh vegetable to eat. We have no problem with vitamin C deficiency. The problem started when human move to colder climate, especially in the winter. There are no fruits or vegetables to eat. Scurvy became the problem that cause those people died from  blood loss through the scorbutic vascular wall. According to their studies in guinea pigs that lack of vitamin C cause deposition of Lp(a), fibrinogens, and later with cholesterol and calcium which will strengthening the arteries so called ATHERIOSCLEROSIS. which believe to be the evolutional metabolic countermeasure for ascobate deficiency in order to prevent bleeding to dead. However the guinea pigs feed with good source of vitamin C and proteins had no ATHERIOSCLEROSIS. Their concluded  that chronic lack of Vitamin  C is the primary cause of ATHERIOSCLEROSIS by deposition of Lp(a),fibrinogens, follow by depositions of cholesterol and calcium at the end stage. By supply adequate vitamin C and Protein especially PROLINE AND LYSINE will prevent inflammation of the arteries and eventually will prevent ATHERIOSCLEROSIS to occur. To learn more please click on the study report “Unified Theory of Human Cardiovascular Disease Leading the Way to the Abolition of This Disease as a Cause for Human Mortality” http://www.orthomed.org/links/papers/rathpau.htm

and Dr. Rath website here

http://www.drrathresearch.org/clinical_studies/condition_atherosclerosis.html

http://www.lbl.gov/Science-Articles/Archive/pauling-and-vitamin-c.html

http://www.vitamincfoundation.org/unified.htm

http://academic.evergreen.edu/c/cahdea07/Research.htm

http://www.mercola.com/2001/mar/28/linus_pauling.htm

http://www.medical-library.net/sites/framer.html?/sites/_vitamin_c_and_vascular_disease.html

THE HUMAN DEFECT  # 2 Unable to produce enzyme lactase to digest milk after a few years after birth cause medical condition called  LACTOSE INTOLERANCE(click here for definitionhttp://en.wikipedia.org/wiki/Lactose_intolerance )

All newborn mammals depend on their mother’s milk to survive at least for the first few days to a year. Why majority of people on this earth (up to 75 percent)(click here for the incidence worldwidehttp://anthro.palomar.edu/adapt/adapt_5.htm )unable to tolerate milk?(to lean more clickhttp://www.indiana.edu/~ensiweb/lessons/tp.milk3.html ) This is a good question.

The milk is mainly sugar(lactose or galactose+ glucose), proteins, fat

Click here for milk composition http://classes.aces.uiuc.edu/AnSci308/milkcomp.html

The fact is after weaning period we are no longer need milk to keep as a primary food source. The small intestine now no longer produce adequate enzyme LACTASE usually occurs two to three years after birth. So lack of enzyme lactase in human is normal. For the people who develop lactose tolerance actually is abnormal due to mutation of the gene on chromosome 2 during human evolution around ten thousand years ago when people in Europe (Nomadic tribe) started raise domestic animal such as cow and goat.

to obtain milk for food These people somehow their intestinal track continue to maintain production of lactase through their adult life and pass on this gene to their off springs.

Only a few minority groups of people that carry this gene include northern Europe (Sweden) and southern Sudan in Africa which has very low incidence of lactose intolerance(4 % and  17 % respectively)

            In the same lactose tolerance population from northern Europe also found that they also have another survival gene that produce special protein that help carry fat called APOLIPROPROTEIN E4 (APOE4) which help absorb cholesterol from food more than other population that have lactose intolerance and carry different apoliproproteins (E2, E3) in order to survive during famine period. So definitely this group of high serum APO E4 will have higher incidence of cardiovascular disease.

In conclusion milk is not our natural food as far as human evolution is concern and possible the one who can drink milk might increase chance to have circulation problem than other people who can’t.

To learn more please click here

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11726725&dopt=Abstract

http://www.cmj.org/information/full.asp?id=856

http://jcem.endojournals.org/cgi/content/abstract/87/9/4147

Or you can read “Genetic Nutrition” by A. P. Simopoulos, M.D.

THE HUMAN DEFECT  # 3 Our thrifty gene that keep us alive now exact the same gene that are killing us

            You probably learn more in the news lately about obesity epidemic in this country about 60 percent of the population either overweight or obese. The simple reason is we eat more than we need. At the same time diabetes incident also increase. I believe every one on this earth has a good chance to have diabetes if we become obese and live long enough because we all carry the thrifty gene that keep us alive for million of years.

Evolution of thrifty gene and diabetes

            The “ thrifty gene” theory proposed in 1962 by geneticist James Neel. Why many Pima Indians are overweight and have the highest incidence of type two diabetes(67 % for male and 73 % for female aged over 45). Because of this gene that make these people survive the famine. This thrifty gene work this way, due to inadequate food intake in order to survive this famine period. The evolutional pressure and natural  selection to survive cause our gene to mutate and make our cells to resist to insulin hormone. The hormone that cause low blood sugar, the hormone that help to transfer the nutrients (fat, carbohydrate and protein) into the cells and help convert all nutrient to storage as fat(we also call the  insulin “the fat storage hormone” ), as well as prevent fat to be used as energy. Normally if you have too much insulin it will reduce the blood sugar. If the blood sugar is too low it will make you sick; weak shaky, sweating unable to concentrate and even death, this low blood sugar or hypoglycemia also signal you to eat more. When the body become resist to insulin. You now will no longer hungry and less sick without food during famine period. However during feast period because of high insulin level the nutrients will convert to fat for storage for the future use at the higher rate.This people who carry this gene will be fatter and have better chance to survive during famine period. Now, at the present because we eat more calories more than the body  need we become obese and overweight that even make our cells more resist to insulin especially the viscera fat in our abdomen which produce the chemical that make  our cells even more resist to insulin. This situation creates a lot of stress to the pancreas to produce even more insulin in order to maintain the normal blood sugar. Eventually the Pancreas cells (Beta cells) will be exhausted and fail and unable to supply the insulin that cause high blood sugar to rise above normal or diabetes.

The Pima Indian evolution

            According to “ Out of Africa theory” We as a Homo sapiens are very homogenous species. Only skin color (which merely an evolutionary response to ultraviolet radiation in sunlight) that separate us as racial differences. We, over 6 billions people on this earth are counsins. We had the same ancestor in Africa who created us 250,000 years ago.

            These same people migrated out of Africa about 100,000 years ago and started migrating all over the world. A group of people called Mongoloid race from northern Asia crossed the Beringia about 15,000 to 35,000 years ago and later on, these peoples were mistakenly called Indians by Christopher Columbus. 11,000 years ago we occupied all the corners of the earth included South America except Antactica.

            The American Pima Indian in Arizona had been lived in this area for about 2000 years. The ancestors of the American Pima Indians migrated from Mexico around 300 B.C. In 1940 the occurrence of diabetes was almost unknown. At the present time up to 75 % of certain segment of population of American Pima Indians have diabetes and 95 % of those with diabetes are overweight.(compared with Mexican Pimas  3 out of 35 had diabetes and the population as a whole was not overweight).

In my opinion : All of us carry this thrifty gene if we allow ourselves to get fat, over time we will have diabetes

To learn more about the subject please click the links below

ANTHROPOLOGY: http://faculty.ncwc.edu/toconnor/soc/355lect02.htm

Obesity and diabetes inPima Indian:

http://diabetes.niddk.nih.gov/dm/pubs/pima/obesity/obesity.htm

Diabetes in Indian population:

http://www.as.ua.edu/ant/bindon/ant570/Papers/King/king.htm

The thrity gene and Pima Indian:http://www.pbs.org/saf/1110/features/fighting.htm

The thrity gene:

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=10447513

The visceral fat and diabetes:

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12196439&dopt=Abstract

The cause of type 2 diabetes:http://www.well-connected.com/report.cgi/000060_2.htm.

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