Acetylcholine/Choline Deficiency in Chronic Illness – mental, liver, kidney, heart and hormones

Acetylcholine/Choline Deficiency in Chronic Illness – The Hunt for the Missing Egg.

Those who lack choline are prone to mental illness, heart disease, fatty liver and/or hemorrhagic kidney necrosis and chronic illness as choline is oxidized to betaine which acts as an important methyl donor and osmolyte. With fatty liver, a person can be prone to diabetes and other chronic illness.  Eggs are rich in choline.  Choline is also found in a wide range of plant foods in small amounts. Eating a well-balanced vegan diet with plenty of whole foods should ensure you are getting enough choline. Soymilk, tofu, quinoa, and broccoli are particularly rich sources.

Eggs are an excellent source of choline and selenium, and a good source of high-quality protein, vitamin D, vitamin B12, phosphorus andriboflavin. In addition, eggs are rich in the essential amino acid leucine(one large egg provides 600 milligrams), which plays a unique role in stimulating muscle protein synthesis.

ucm278430We hear a lot about vitamins and minerals such as B12, folate, magnesium, vitamin C, and so on, but there seems very little talk these days on the importance of dietary lecithin and choline. Are you consuming an adequate amount of acetylcholine, or other phospholipids? The odds are that you are not.

A little bit about choline

The human body produces choline by methylation of phosphatidylethanolamine (from dietary sources such as lecithin and others) to form phosphatidylcholine in the liver by the PEMT enzyme. Phosphatidylcholine may also be consumed in the diet or by supplementation. Choline is oxidized to betaine which acts as an important methyl donor and osmolyte.

For those wanting to see how this relates to the methylation cycle, below is a nice graphic (courtesy of Wikipedia).

Choline metabolism

It is well known that magnesium deficiency is widespread (57% of the population does not meet the U.S. RDA according to the USDA), but the numbers for choline deficiency are even more shocking.

According the National Health and Nutrition Examination Survey (NHANES) in 2003-2004, only about 10% of the population have an adequate intake of choline. This means about 90% of the population consumes a diet deficient in choline. Furthermore, those without an adequate intake of choline may not have symptoms.

Along with folate and B12 deficiency, inadequate consumption of choline can lead to high homocysteine and all the risks associated with hyperhomocysteinaemia, such as cardiovascular disease, neuropsychiatric illness (Alzheimer’s disease, schizophrenia) and osteoporosis. Inadequate choline intake can also lead to fatty liver or non-alcoholic fatty liver disease (NAFLD).

The most common symptoms of choline deficiency are fatty liver and/or hemorrhagic kidney necrosis. Consuming choline rich foods usually relieve these deficiency symptoms. Diagnosing fatty liver isn’t as simple as running  ALT and AST since nearly 80% of people with fatty liver have normal levels of these enzymes according to a population study published in the journal Hepatology. In fact, in an experiment, 10 women were fed a diet low in choline. Nine developed fatty liver and only one had elevated liver enzymes.


Estrogen and Choline Deficiency

Given the connection between low lipids and choline deficiency, it would be tempting to think that as long as someone has enough cholesterol and TG that they will be protected from choline deficiency.  Unfortunately this is not the case.  Having adequate lipids does indeed help support healthy choline levels, but it does not guarantee a person will avoid choline deficiency.  The truth is that choline deficiency can come from more than one source.  Both sex hormone levels and genetic SNPs may lead to a choline deficiency by influencing the PEMT enzyme – the enzyme responsible for synthesis of choline inside the body.  Recent research now confirms how hormones and genetic polymorphisms play a major role in choline deficiency.

The body can make choline only one way; that is by methylating a molecule of phosphatidylethanolamine (PE) into a molecule of phosphatidylcholine (PC).  The body’s only method for accomplishing this is via the enzyme PEMT (phosphatidylethanolamine N-methyltransferase) which is found in the liver, brain, muscle, fat and other tissues.1,2    As with other well-known methylation enzymes like MTHFR and COMT, the PEMT enzyme can have genetic SNPs that slow it down.  When this enzyme slows down the body cannot make choline in high amounts and choline deficiency is more likely.  But there is more to the story of PEMT than just polymorphisms.  In addition to being slowed by SNPs, PEMT is also dependent upon the hormone estrogen for activation. 1, 3  What this means is that the PEMT enzyme, the body’s only method of synthesizing choline, has not one but two Achilles heals.  The PEMT pathway and how it relates to phosphatidylcholine production is shown in Figure 1.3 below.

Communicating Vessels4-PEMT

Figure 1.3 – PEMT is shown as the rate-limiting reaction in the production of phosphatidylcholine inside the human body.  Due to genetic and hormonal variances, most people have a PEMT enzyme working too slow and are susceptible to choline deficiency when there is not enough choline in the diet.  ACoA – Acetyl-CoA; TG – Triglycerides; PE – phosphatidylethanolamine; PC – phosphatidylecholine; PEMT – phosphatidylethanolamine N-methyltransferase.

As mentioned above, the sex hormone estrogen is intimately linked with the production of choline.  Women have a biological advantage here as the premenopausal female body has much higher levels of estrogen than does the male body.  When a woman becomes pregnant this advantage is taken to an extreme, as pregnancy increases estrogen levels over 30 times normal.4  A successful pregnancy requires high amounts of nutrients delivered to the growing baby, esp. choline.  Since the mother’s body is building a human being from scratch, there is an added burden on her biology to provide enough nutrition to her growing baby.  Viewed from this perspective, the high estrogen levels during pregnancy can be seen to act like a biochemical insurance policy.  Since the PEMT enzyme requires estrogen to function, pregnancy allows a woman to make extra choline for her developing child.  Furthermore, the nervous system is the first system to form in utero and is a tissue that requires high levels of choline for proper development.5, 6  Choline plays such an important role in cell membranes, myelin sheaths, and nervous system tissue that the high estrogen levels during pregnancy help make sure the growing brain and nervous system is nourished.  It is a genius system that assures the health and survival of the child.

Even though Nature has conferred an advantage to females by providing them with higher estrogen levels, esp. during pregnancy, this alone cannot protect against a lack of choline in the diet.  All the estrogen in the world will not save a woman from choline deficiency if the gene responsible for producing choline is slowed down by a polymorphism.  Genetic research has shown that the gene responsible for synthesizing choline, the PEMT gene, is susceptible to common polymorphisms which alter its function by slowing it down.  In a recent study looking at a population in North Carolina, men and women of various ages were placed on a choline-deficient diet.  They were followed closely for up to 42 days on a low choline diet consisting of less than 50mg choline per day.  Throughout the study, the participants’ liver function was continuously assessed for any sign of fatty liver and damage.  After eating a choline deficient diet for just six weeks, 63% of participants developed liver dysfunction and choline blood levels dropped 30% in every single participant, including premenopausal females.7  During this six week trial of low dietary choline the odds of developing liver dysfunction were 77% for men, 80% for postmenopausal women and just 44% for premenopausal women.7  Based on what has been discussed so far about estrogen and choline, it makes sense that men and postmenopausal women would be more susceptible to developing fatty liver since they don’t have high estrogen levels.  And based on the fact that estrogen levels drive choline production, premenopausal women should have been protected from fatty liver since they make higher amounts of choline – but that was not the case.

With dietary choline restricted to just 50 mg/day, approximately half of the premenopausal group also suffered liver dysfunction, suggesting that a choline deficient diet can even harm women with higher estrogen levels.  In addition, blood tests revealed that premenopausal female experienced a 30% loss of choline on a low choline diet right along with everyone else.   Despite the fact that higher estrogen levels allow fertile women to make more choline, many were not able to make enough to avoid problems.  A PEMT gene polymorphism is the only mechanism that can explain how women with high estrogen levels are still susceptible to choline deficiency when placed on a low choline diet.

Just like many individuals in the population, some of the premenopausal women inherited one or two copies of the PEMT gene which slows down the production of choline.   This study showed that fatty liver occurred in 80% of the premenopausal women with two copies of PEMT and in 43% with only one copy of PEMT.8  What this means is that a premenopausal woman with two copies of the slowed PEMT gene has exactly the same risk of fatty liver as a postmenopausal woman.  It is as if inheriting two copies of the PEMT gene effectively shuts off all estrogen-related choline production in the body.  If a woman only has a single copy of the slowed PEMT gene, she will still have a roughly 50% chance of liver dysfunction on a low choline diet.  Thus a single copy of the gene is only slightly better than two copies, as at least some estrogen-related choline production is preserved.

If having a PEMT gene can put one at risk for choline-related diseases like fatty liver, then it is important to know how common these genes are in population.  We know that 74% of all women in the study had a SNP in the PEMT that made their PEMT enzyme unresponsive to estrogen.9  This means that only 26% of women can make enough choline on a low choline diet; and that ability depends on whether the woman is still fertile or has entered menopause.  In this way genetics can take away the biological advantage that high estrogen levels usually offer to premenopausal females.  Women with these PEMT genes will be at risk for choline deficiency and liver damage just like all men and post-menopausal women – two groups who don’t have enough estrogen to make choline regardless of their genes.  Due to all the interference from the PEMT gene, dietary choline levels must be optimized for the vast majority of our population.

Summary of PEMT and Choline Deficiency:

  • In humans, choline is only made by the PEMT enzyme
  • Estrogen is required for the PEMT enzyme to activate and function normally
  • Men and postmenopausal women have an elevated risk of choline deficiency due to low estrogen levels.
  • The PEMT enzyme is commonly slowed down by polymorphisms, making it unresponsive to estrogen levels
    • 74% of women have at least one copy of a slowed PEMT
    • Homozygous carriers of PEMT have much higher risk of choline deficiency
    • Men, postmenopausal women, and premenopausal women with PEMT SNPs need to increase choline intake in the diet to offset elevated risk of liver dysfunction

The take away here is that studies have recently shown that because of common genetic polymorphisms, choline deficiency is a widespread problem.  Normally the hormone estrogen allows the body to make choline from scratch.  However, genetic variation in the PEMT enzyme, estrogen levels and gender differences prevent most people from making adequate choline.  Realistically then the only group in our population who is protected from choline deficiency are premenopausal females without a single copy of the slowed PEMT gene.   Every single male, every single postmenopausal woman, and 74% of premenopausal woman all require daily intake of approx. 500 mg of choline to prevent fatty liver, organ damage, and the associated health problems.7  If the body is already depleted, then levels that simply prevent deficiency won’t be enough to replete the body.  In these cases, higher daily doses of at least 1 gram or more are needed to replenish the tissues.  Choline it seems must be absorbed from the diet in just about everyone except for the few young women who have a normal PEMT gene and can synthesize choline regardless of dietary intake.

References

1 Resseguie ME, da Costa KA, Galanko JA, et al. Aberrant estrogen regulation of PEMT results in choline deficiency-associated liver dysfunction. J Biol Chem. 2011 Jan 14;286(2):1649-58.

2 Tehlivets O. Homocysteine as a risk factor for atherosclerosis: is its conversion to s-adenosyl-L-homocysteine the key to deregulated lipid metabolism? J Lipids. 2011;2011:702853. Epub 2011 Aug 1.

3 Wallace JM, McCormack JM, McNulty H, et al. Choline supplementation and measures of choline and betaine status: a randomised, controlled trial in postmenopausal women. Br J Nutr. 2012 Oct;108(7):1264-71. Epub 2011 Dec 15.

4 Guyton AC, Hall JE. Textbook of Medical Physiology, 11th ed.  Philadelphia, PA: Elsevier, 2006, p. 1033.

5 Sadler, TW. Medical Embryology, 10th ed. Baltimore, MD: Lippincott Williams & Wilkins, 2006, p. 86.

6 Steinfeld R, Grapp M, Kraetzner R, et al. Folate Receptor Alpha Defect Causes Cerebral Folate Transport Deficiency: A Treatable Neurodegenerative Disorder Associated with Disturbed Myelin Metabolism. Am J Hum Genet. 2009 September 11; 85(3): 354–363.

7 da Costa KA, Kozyreva OG, Song J, et al. Common genetic polymorphisms affect the human requirement for the nutrient choline. FASEB J. 2006 Jul;20(9):1336-44.

8 Fischer LM, da Costa KA, Kwock L, et al. Dietary choline requirements of women: effects of estrogen and genetic variation. Am J Clin Nutr. 2010 Nov;92(5):1113-9. Epub 2010 Sep 22.

9 Zeisel SH. Nutritional genomics: defining the dietary requirement and effects of choline. J N

What have been the advantages of humans acquiring Neanderthal genes?

neand

https://clubalthea.com/2016/10/20/what-makes-the-inherited-genetic-material-beneficial/

When Neanderthal ancestors left Africa roughly 100,000 years earlier they adapted to the pathogens in their European environment, unlike modern humans who adapted to African pathogens. This transcontinental movement is known as the Out of Africa model. If contact between humans and Neanderthals occurred in Europe and Asia the first contact may have been devastating to the Neanderthal population, because they would have had little if any immunity to the African pathogens. More recent historical events in Eurasia and the Americas show a similar pattern, where the unintentional introduction of viral, or bacterial pathogens to unprepared populations has led to mass mortality and local population extinction.

The most well-known example of this is the arrival of Christopher Columbus to the New World, which brought and introduced foreign diseases when he and his crew arrived to a native population who had no immunity.

Anthropologist Pat Shipman, of Pennsylvania State University, suggested that domestication of the dog could have played a role in Neanderthals’ extinction.

Polymorphism is common in nature; it is related to biodiversity, genetic variationand adaptation; it usually functions to retain variety of form in a population living in a varied environment.

The most common example is sexual dimorphism, which occurs in many organisms. Other examples are mimetic forms of butterflies (see mimicry), and human hemoglobin and blood types.

According to the theory of evolution, polymorphism results from evolutionary processes, as does any aspect of a species. It is heritable and is modified by natural selection. In polyphenism, an individual’s genetic make-up allows for different morphs, and the switch mechanism that determines which morph is shown is environmental. In genetic polymorphism, the genetic make-up determines the morph. Ants exhibit both types in a single population.

Why does our skin causing us to age?

epi-mechskin-epi

Epigenetics studies genetic effects notencoded in the DNA sequence of an organism, hence the prefix epi- (Greek: επί– over, outside of, around).[1][2] Such effects on cellular and physiological phenotypic traits may result from external or environmental factors that switch genes on and off and affect how cells express genes.[3][4] These alterations may or may not be heritable, although the use of the term epigenetic to describe processes that are heritable is controversial.[5]

The term also refers to the changes themselves: functionally relevant changes to the genome that do not involve a change in the nucleotide sequence. Examples of mechanisms that produce such changes are DNA methylationand histone modification, each of which alters how genes are expressed without altering the underlying DNA sequence. Gene expression can be controlled through the action of repressor proteins that attach to silencer regions of the DNA. These epigenetic changes may last through cell divisions for the duration of the cell’s life, and may also last for multiple generations even though they do not involve changes in the underlying DNA sequence of the organism;[6] instead, non-genetic factors cause the organism’s genes to behave (or “express themselves”) differently.[7]

 


Connie’s skin tips: Sleep, hydrate, moisturize, use Vit C serum (DIY), wash with lemon and left over tea bags and apply sunscreen (from whole foods store).

https://clubalthea.com/2014/02/23/stop-aging-of-your-face-with-diy-vitamin-c-serum-by-wellnessmama/

Gene-based diet weekly schedule

Gene-based heart healthy recipe

A personalized recipe recommendations to meet your dietary needs and preferences.

Notes for Sunday and Saturday prep tips: Seek farmer’s market produce, cut fruits/veggies in cubes and store in portion bag in freezer for Mon-Friday smoothie, soup, or steamed veggie recipe.  If you cook a big batch of chicken or beef broth soup, store in freezer some portion (liquid) to be added to soups later.

Ingredient lists for shopping

Organic chicken or beef meat with bones, onions, garlic, carrots, celery, cilantro, yams, plantain banana, potatoes, wild salmon (broiled with rosemary and ginger), ginger, bell pepper, mushrooms,parsley,bay leaf,thyme

Heart healthy soup

heart-soup

Prep tips

Make a broth from chicken or beef bones and divide into portion and store half of the liquid for future use in soups. Add more onions, carrots, celery and garlic and use a blender for easy digestion for seniors or babies. Be sure to throw bones before serving. Always start with sauteiing garlic and onions and meat before adding other ingredients and water for the soup. Broiled wild salmon with garlic, ginger, salt and onions, serve with brown rice and chicken or beef broth soup.

Schedule tips

Saturday, Sunday and Wed

Health benefits of ingredients

Omega 3, Vit E and D, Vit C, magnesium and calcium, potassium-rich, sulfur-rich

And more…..

Gene-based immune system healthy recipe

Ingredient lists for shopping

Picture

Prep tips

Schedule tips

Health benefits of ingredients: Sulfur-rich foods, Vit C rich, zinc and Vitamin D, greens, rich in potassium, phosporous, omega 3 and greens

Gene-based circulatory system healthy recipe

Ingredient lists for shopping

Picture

Prep tips

Schedule tips

Health benefits of ingredients: Ginger, onions and garlic, red and green colored whole foods, good fats (avocado and walnuts),

Gene-based cleansing system for liver and kidneys healthy recipe

Ingredient lists for shopping

Picture

Prep tips

Schedule tips: Served daily in small portions

Health benefits of ingredients: Lemon for cleansing, garlic, onions and sulfur rich (yellow) foods, more soups, less on raw foods (greens are half cooked), and all foods consumed between 11am to 8pm.

Gene-based regenerating healthy recipe

Ingredient lists for shopping

Picture

Prep tips

Schedule tips

Health benefits of ingredients: Yellow and red colored whole foods, pickled veggies, good protein (softer), whole foods (mostly cooked-not over cooked)

Gene-based wholesome for the teens healthy recipe

Ingredient lists for shopping

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Prep tips

Schedule tips

Health benefits of ingredients: more on healthy carbs (yams), protein rich and equal amount of good fats (avocado, walnuts,others)


Please email any suggested recipes to motherhealth@gmail.com

 

 

Contributing factors to aging

aging-genes-3aging-genes-2aging-genes-1
It has been a long standing goal to develop molecular biomarkers of biological age. Recent studies demonstrate that powerful epigenetic biomarkers of aging can be defined based on DNA methylation levels. For example, the epigenetic clock (PMID: 24138928) is a multivariate age estimation method that applies to sorted cell types (CD4T cells or neurons), complex tissues, and organs and even prenatal brain samples. The epigenetic clock is an attractive biomarker of aging because a) it applies to most human and chimpanzee tissues, b) its accurate measurement of chronological age is unprecedented, c) it is predictive of all-cause mortality even after adjusting for a variety of known risk factors, d) it correlates with measures of cognitive and physical fitness in the elderly, and e) it has been found useful for detecting accelerated aging effects due to obesity, Down syndrome, and HIV infection. Recent genomewide association studies shed light on the underlying biological mechanisms.

For more information go to https://oir.nih.gov/wals

Author: Steve Horvath, Sc.D., Ph.D., University of California, Los Angeles

Permanent link: http://videocast.nih.gov/launch.asp?1…

Colorectal, ovarian-uterine, prostate, kidney, liver and bladder cancer risk Factor

COPKL: Colorectal, ovarian/uterine, prostate, kidney, liver and bladder cancer risk Factor, formula by Connie Dello Buono , ©12Sept2016

Assumption: Female/Male, over 50yrs of age, on western diet, lives in Northern hemisphere, have families with cancer, diabetes and polyps, prone to allergies (lack zinc), digestive disorders, high dairy and sugar consumption (low magnesium and calcium,iron) and had used some medications in the past

COPKL Risk Factor = Blood sugar (0.2) + history (0.1) + sugar/processed foods consumption (0.1) + Exercise and sun exposure (0.1) + number of medications (0.1) + obesity/night time worker (0.1) + exposure to copper,fungus,molds,aflatoxins (0.1) + genes (0.2)

  • COPKL Risk Factor =1.0 (High)
  • COPKL Risk Factor = 6- 4 (Medium)
  • COPKL Risk Factor = < 3 (Low)

Please email your entries to motherhealth@gmail.com to create a database and get health data insights on Prostate,Colorectal,kidney,liver and ovarian/uterine disease.

Modified Colon and other cancer risk factor

Blood sugar
Normal/low =0High = 0.2
Med =0.1
Previous history of cancer/bowel disease, family cancer/polyps
Normal/low=0
High = 0.1
Race = 0.1 racial/ethnic background (African American, Eastern European Jews)
Exercise and sun exposure, 3x per week = 0
No exercise = 0.1
Exposure to copper,fungus,molds,toxins, smoking,alcohol,narcotics, aluminum, air pollution, char broiled meat, aflatoxin, virus,bacteria, medications > 5
(H,M,L)
Yes = H,M = 0.1
Metabolic and diet:
Diabetes 0.1Night time work, obesity (H,M,L)
H = 0.1
Age > 45 yrs old Genes:
0.2 = MSH2, MLH1, MSH6, PMS2, PMS1, TGFBR2, MLH3 , RCC, APC, HPC1, tmprss2-erg ,  TMPRSS2-ETV1/4, HBOC,BRCA,BRCA2,BRCA1
(0.2 more than 2 genes, 0.1 one gene),
Weak immune and metabolic system:
Infection and allergy 0.1
 

colo-rectal-kidney-cancer-risk-factors

risk-factor

Having an inherited syndrome

About 5% to 10% of people who develop colorectal cancer have inherited gene defects (mutations) that can cause family cancer syndromes and lead to them getting the disease. The most common inherited syndromes linked with colorectal cancers are familial adenomatous polyposis (FAP) and Lynch syndrome (hereditary non-polyposis colorectal cancer, or HNPCC), but other rarer syndromes can also increase colorectal cancer risk.

Familial adenomatous polyposis (FAP): FAP is caused by changes (mutations) in the APC gene that a person inherits from his or her parents. About 1% of all colorectal cancers are due to FAP.

In the most common type of FAP, hundreds or thousands of polyps develop in a person’s colon and rectum, usually in their teens or early adulthood. Cancer usually develops in 1 or more of these polyps as early as age 20. By age 40, almost all people with this disorder will have developed colon cancer if the colon isn’t removed first to prevent it. People with FAP are also at increased risk for cancers of the stomach, small intestines, and some other organs.

In attenuated FAP, which is a subtype of this disorder, patients have fewer polyps (less than 100), and colorectal cancer tends to occur at a later age.

Gardner syndrome is a type of FAP that also has non-cancerous tumors of the skin, soft tissue, and bones.

Lynch syndrome (hereditary non-polyposis colon cancer, or HNPCC): Lynch syndrome accounts for about 2% to 4% of all colorectal cancers. In most cases, this disorder is caused by an inherited defect in either the MLH1 or MSH2 gene, but changes in other genes can also cause Lynch syndrome. These genes normally help repair DNA damage. (See Do we know what causes colorectal cancer? for more details.)

People with this syndrome develop cancers when they are relatively young, although not as young as in FAP. People with Lynch syndrome may have polyps, but they tend to only have a few, not hundreds as in FAP. The lifetime risk of colorectal cancer in people with this condition may be as high as 80%, although this depends on which gene is affected.

Women with this condition also have a very high risk of developing cancer of the endometrium (lining of the uterus). Other cancers linked with Lynch syndrome include cancer of the ovary, stomach, small intestine, pancreas, kidney, brain, ureters (tubes that carry urine from the kidneys to the bladder), and bile duct.

For more information on Lynch syndrome, see Do we know what causes colorectal cancer? and Can colorectal cancer be prevented?

Turcot syndrome: This is a rare inherited condition in which people have a higher risk of adenomatous polyps and colorectal cancer, as well as brain tumors. There are actually 2 types of Turcot syndrome:

One is caused by gene changes similar to those seen in FAP, in which cases the brain tumors are medulloblastomas.

The other is caused by gene changes similar to those seen in Lynch syndrome, in which cases the brain tumors are glioblastomas.

Peutz-Jeghers syndrome: People with this rare inherited condition tend to have freckles around the mouth (and sometimes on the hands and feet) and a special type of polyp in their digestive tracts (called hamartoma). These people are at greatly increased risk for colorectal cancer, as well as several other cancers, which usually appear at a younger than normal age. This syndrome is caused by mutations in the STK1 gene.

MUTYH-associated polyposis: People with this syndrome develop colon polyps which will become cancerous if the colon is not removed. These people also have an increased risk of cancers of the small intestine, skin, ovary, and bladder. This syndrome is caused by mutations in the MUTYH gene.

These syndromes often lead to cancer at a younger age than is usual. They are also linked to some other types of cancer. Identifying families with these inherited syndromes is important because it lets doctors recommend specific steps such as screening and other preventive measures when the person is younger.

Information on risk assessment, and genetic counseling and testing for these syndromes can be found in Colorectal Cancer Prevention and Early Detection.

Your racial and ethnic background

African Americans have the highest colorectal cancer incidence and mortality rates of all racial groups in the United States. The reasons for this are not yet understood.

Jews of Eastern European descent (Ashkenazi Jews) have one of the highest colorectal cancer risks of any ethnic group in the world. Several gene mutations leading to an increased risk of colorectal cancer have been found in this group. The most common of these gene changes, called the I1307K APC mutation, is present in about 6% of American Jews.

Having type 2 diabetes

People with type 2 (usually non-insulin dependent) diabetes have an increased risk of colorectal cancer. Both type 2 diabetes and colorectal cancer share some of the same risk factors (such as being overweight or obese). But even after taking these factors into account, people with type 2 diabetes still have an increased risk. They also tend to have a less favorable prognosis (outlook) after diagnosis.

Factors with unclear effects on colorectal cancer risk

Night shift work

Results of one study suggested working a night shift at least 3 nights a month for at least 15 years may increase the risk of colorectal cancer in women. The study authors suggested this might be due to changes in levels of melatonin (a hormone that responds to changes in light) in the body. More research is needed to confirm or refute this finding.

Previous treatment for certain cancers

Some studies have found that men who survive testicular cancer seem to have a higher rate of colorectal cancer and some other cancers. This might be because of the treatments they have received.

Several studies have suggested that men who had radiation therapy to treat prostate cancer might have a higher risk of rectal cancer because the rectum receives some radiation during treatment. Most of these studies are based on men treated in the 1980s and 1990s, when radiation treatments were less precise than they are today. The effect of more modern radiation methods on rectal cancer risk is not clear.


Calculate your Alzheimer’s risk factor

https://clubalthea.com/2016/09/12/alzheimers-disease-data-insigths/

Calculate your Blood cancer risk factor

https://clubalthea.com/2016/09/16/prenatal-health-of-mother-may-contribute-to-childhood-leukemia/


Join 25,000 people in helping redefine health with health concierge and precision medicine.

https://clubalthea.com/2016/10/14/your-complete-dna-sequence-will-help-shape-the-future-of-medicine/

Antisocial personality disorder in 70% of prison inmates

Antisocial personality disorder

Antisocial personality disorder (ASPD), also known as dissocial personality disorder (DPD) and sociopathy, is apersonality disorder, characterized by a pervasive pattern of disregard for, or violation of, the rights of others.

Prisoners

An international team of Finnish, American, British, and Swedish researchers examined data from the Finnish CRIME sample — a database of psychological tests and genetic material from 794 Finnish prisoners taken between 2010-2011.

The findings of this study cannot be implemented for any prediction purposes, or brought into courthouses to be given any legal weight.
Of the 794 prisoners, a full 568 screened positive for ASPD. By comparing that group’s genetic material to a large control sample from the general population, the researchers identified a number of genes that may play a role in at least some ASPD cases.

Hormones and neurotransmitters

Traumatic events can lead to a disruption of the standard development of the central nervous system, which can generate a release of hormones that can change normal patterns of development.[36] Aggressiveness and impulsivity are among the possible symptoms of ASPD. Testosterone is a hormone that plays an important role in aggressiveness in the brain.[37] For instance, criminals who have committed violent crimes tend to have higher levels of testosterone than the average person.[37] The effect of testosterone is counteracted by cortisol which facilitates the cognitive control on impulsive tendencies.[37]

One of the neurotransmitters that have been discussed in individuals with ASPD is serotonin, also known as 5HT.[36] A meta-analysis of 20 studies found significantly lower 5-HIAA levels (indicating lower serotonin levels), especially in those who are younger than 30 years of age.[38]

J.F.W. Deakin of University of Manchester‘s Neuroscience and Psychiatry Unit has discussed additional evidence of a connection between 5HT (serotonin) and ASPD. Deakin suggests that low cerebrospinal fluid concentrations of 5-HIAA, and hormone responses to 5HT, have displayed that the two main ascending 5HT pathways mediate adaptive responses to post and current conditions. He states that impairments in the posterior 5HT cells can lead to low mood functioning, as seen in patients with ASPD. It is important to note that the dysregulated serotonergic function may not be the sole feature that leads to ASPD but it is an aspect of a multifaceted relationship between biological and psychosocial factors.[citation needed]

While it has been shown that lower levels of serotonin may be associated with ASPD, there has also been evidence that decreased serotonin function is highly correlated with impulsiveness and aggression across a number of different experimental paradigms. Impulsivity is not only linked with irregularities in 5HT metabolism but may be the most essential psychopathological aspect linked with such dysfunction.[39] Correspondingly, the DSM classifies “impulsivity or failure to plan ahead” and “irritability and aggressiveness” as two of seven sub-criteria in category A of the diagnostic criteria of ASPD.[19]

Some studies have found a relationship between monoamine oxidase A and antisocial behavior, including conduct disorder and symptoms of adult ASPD, in maltreated children.[citation needed]

Head injuries

Researchers have linked physical head injuries with antisocial behavior.[40][41][42] Since the 1980s, scientists have associated traumatic brain injury, including damage to the prefrontal cortex, with an inability to make morally and socially acceptable decisions.[40][42] Children with early damage in the prefrontal cortex may never fully develop social or moral reasoning and become “psychopathic individuals … characterized by high levels of aggression and antisocial behavior performed without guilt or empathy for their victims.”[40][41] Additionally, damage to the amygdala may impair the ability of the prefrontal cortex to interpret feedback from the limbic system, which could result in uninhibited signals that manifest in violent and aggressive behavior.[40]

Family environment

Some studies suggest that the social and home environment has contributed to the development of antisocial behavior. The parents of these children have been shown to display antisocial behavior, which could be adopted by their children.

Source: Wiki

Cortisol, serotonin and depression: all stressed out?

The fact that patients with major depression exhibit decreased brain serotonin (5-hydroxytryptamine, 5-HT) function and elevated cortisol secretion has reached the status of textbook truism. More recent formulations have suggested that elevated cortisol levels, probably caused by stressful life events, may themselves lower brain 5-HT function and this in turn leads to the manifestation of the depressive state (see Dinan, 1994). This elegant proposal neatly ties abnormalities of cortisol secretion and 5-HT function into a causal chain in which cortisol is the key biological mediator through which life stress lowers brain 5-HT function, thereby causing depression in vulnerable individuals.

The importance, and occasional discomfort, of testing cherished beliefs is shown in a ground-breaking study from the Manchester University Department of Psychiatry published in this issue of the journal (Strickland et al, 2002). In a large group of women the authors found no evidence of increased salivary cortisol levels in those with depression or in the majority of those vulnerable to depression through adverse social or personal circumstances. Moreover, in women with depression, brain 5-HT function (as judged by the prolactin response to the 5-HT releasing agent, d-fenfluramine) was increased rather than diminished. These findings pose serious problems for hypotheses linking hypercortisolaemia with lowered brain 5-HT function and depression.

Source: http://bjp.rcpsych.org/content/180/2/99


Massage therapy on cortisol and serotonin

In this article the positive effects of massage therapy on biochemistry are reviewed including decreased levels of cortisol and increased levels of serotonin and dopamine. The research reviewed includes studies on depression (including sex abuse and eating disorder studies), pain syndrome studies, research on auto-immune conditions (including asthma and chronic fatigue), immune studies (including HIV and breast cancer), and studies on the reduction of stress on the job, the stress of aging, and pregnancy stress. In studies in which cortisol was assayed either in saliva or in urine, significant decreases were noted in cortisol levels (averaging decreases 31%). In studies in which the activating neurotransmitters (serotonin and dopamine) were assayed in urine, an average increase of 28% was noted for serotonin and an average increase of 31% was noted for dopamine. These studies combined suggest the stress-alleviating effects (decreased cortisol) and the activating effects (increased serotonin and dopamine) of massage therapy on a variety of medical conditions and stressful experiences.

http://www.ncbi.nlm.nih.gov/pubmed/16162447

Correlation between cortisol level and serotonin uptake in patients with chronic stress and depression

In a recent study (Tafet, Toister-Achituv, & Shinitzky, 2001), we demonstrated that cortisol induces an increase in the expression of the gene coding for the serotonin transporter, associated with a subsequent elevation in the uptake of serotonin. This stimulatory effect, produced upon incubation with cortisol in vitro, was observed in peripheral blood lymphocytes from normal subjects. In the present work we investigated the cortisol-induced increase in serotonin uptake in lymphocytes from hypercortisolemic patients, including subjects with major depressive disorder (n = 8), and subjects with generalized anxiety disorder (n = 12), in comparison with a control group of normal healthy subjects (n = 8). A significant increase in serotonin uptake (+37% + 14, M + SD) was observed in the control group, whereas neither the generalized anxiety disorder nor the major depression group exhibited changes in serotonin uptake upon incubation with cortisol. It is likely that under chronic stress or depression, the capacity for increase in serotonin transporter has reached its limit due to the chronically elevated blood cortisol level.

http://www.ncbi.nlm.nih.gov/pubmed/12467090


Connie’s comments: A stressed baby can lead to personality disorder in adulthood. Nurture prevents many personality disorders.

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