Vitamin B3, Leukemia, aging and cancer

Grass fed beef, bone marrow with veggie soup, peanuts and chicken are some of the food sources of Vitamin B3.  I take Vitamin Bs when I am under stress and these vitamins help me sleep too. Vitamin B3 is a natural product found in our blood. Will sunshine help clean our blood. There are many ways to have a healthy blood: exercise with sunshine, avoidance of alcohol, drugs and environmental toxins (metals,gas), whole foods, sleep, less stress and a positive spirit (calm not full of anxiety).

Connie

Nicotinamide riboside (NR) is a pyridinenucleoside form of vitamin B3 that functions as a precursor to nicotinamide adenine dinucleotide or NAD+.

NR was first described in 1944 as a growth factor, termed Factor V, for Haemophilus influenza, a bacterium that lives in and depends on blood. Factor V, purified from blood was shown to exist in three forms: NAD+, NMN and NR. NR was the compound that led to the most rapid growth of this bacterium.[5] Notably, H. influenza cannot grow on nicotinic acidnicotinamidetryptophan or aspartic acid, which were the previously known precursors of NAD+.[6]

In 2000, yeast Sir2 was shown to be an NAD+-dependent protein lysine deacetylase,[7] which led several groups to probe yeast NAD+ metabolism for genes and enzymes that might regulate lifespan. Biosynthesis of NAD+ in yeast was thought to flow exclusively through NAMN (nicotinic acid mononucleotide).[8][9][10][11][12]

When NAD+ synthase (glutamine-hydrolysing) was deleted from yeast cells, NR permitted yeast cells to grow. Thus, these Dartmouth College investigators proceeded to clone yeast and human nicotinamide riboside kinases and demonstrate the conversion of NR to NMN by nicotinamide riboside kinases in vitro and in vivo. They also demonstrated that NR is a natural product, a little-noticed vitamin found in cow’s milk.[13][14]

In the 2010s. dietary supplements containing NR were brought to market by ChromaDex under the brand Niagen, which also originally provided NR to Elysium Health which uses NR as a component of its product, Basis.[15]

References

  1. Jump up^ Bogan, K.L., Brenner, C. (2008). “Nicotinic acid, nicotinamide, and nicotinamide riboside: a molecular evaluation of NAD+ precursor vitamins in human nutrition”. Annu. Rev. Nutr28: 115–130. doi:10.1146/annurev.nutr.28.061807.155443.
  2. Jump up^ Chi Y, Sauve AA (November 2013). “Nicotinamide riboside, a trace nutrient in foods, is a vitamin B3 with effects on energy metabolism and neuroprotection”. Curr Opin Clin Nutr Metab Care16 (6): 657–61. doi:10.1097/MCO.0b013e32836510c0PMID 24071780.
  3. Jump up to:a b c “Spherix/Chromadex GRAS submission” (PDF). March 8, 2016. See FDA GRAS index page: “GRAS Notice (GRN) No. 635”.
  4. Jump up^ “Nicotinamide Riboside”.
  5. Jump up^ Gingrich, W (1944). “Codehydrogenase I and other pyridinium compounds as V factor for Haemophilus influenzae and Haemophilus parainfluenzae”. J. Bacteriol47: 535–550.
  6. Jump up^ Belenky, P. et. al. (2007). “NAD+ Metabolism in Health and Disease”. Trends in Biochemical Sciences32: 12–19. doi:10.1016/j.tibs.2006.11.006PMID 17161604.
  7. Jump up^ Imai, S.; et al. (2000). “Transcriptional silencing and longevity protein Sir2 is an NAD-dependent histone deacetylase”. Nature403 (6771): 795–800.
  8. Jump up^ Panozzo, C.; et al. (2002). “Aerobic and anaerobic NAD+ metabolism in Saccharomyces cerevisiae”. FEBS Lett517: 97–102. doi:10.1016/s0014-5793(02)02585-1.
  9. Jump up^ Sandmeier; et al. (2002). “Telomeric and rDNA silencing in Saccharomyces cerevisiae are dependent on a nuclear NAD Salvage Pathway”. Genetics160: 877–889.
  10. Jump up^ Bitterman; et al. (2002). “Inhibition of silencing and accelerated aging by nicotinamide, a putative negative regulator of yeast Sir2 and human SIRT1”. J. Biol. Chem277: 45099–45107. doi:10.1074/jbc.m205670200PMID 12297502.
  11. Jump up^ Anderson; et al. (2003). “Nicotinamide and PNC1 govern lifespan extension by calorie restriction in Saccharomyces cerevisiae”Nature423: 181–185. doi:10.1038/nature01578PMC 4802858Freely accessiblePMID 12736687.
  12. Jump up^ Gallo; et al. (2004). “Nicotinamide clearance by pnc1 directly regulates sir2-mediated silencing and longevity”. Mol. Cell. Biol24: 1301–1312. doi:10.1128/mcb.24.3.1301-1312.2004.
  13. Jump up^ Bieganowki, P. & Brenner, C. (2004). “Discoveries of Nicotinamide Riboside as a Nutrient and Conserved NRK Genes Establish a Preiss-Handler Independent Route to NAD+ in Fungi and Humans”. Cell117: 495–502. doi:10.1016/s0092-8674(04)00416-7PMID 15137942.
  14. Jump up^ Hautkooper, R.H.; et al. (2012). “Sirtuins as regulators of metabolism and healthspan”. Nat. Rev. Mol. Cell Biol13: 225–238. doi:10.1038/nrm3293.
  15. Jump up^ Zhang, Sarah (July 6, 2016). “The weird business behind a trendy “anti-aging” pill”Wired.

MS drug may be linked to increased risk of leukemia and colorectal cancer

cancer cells

Sugar , transfat and poor lifestyle – causes of American death in last 35 years

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Smoking , alcohol, meds/drugs and poor lifestyle (absence of exercise, clean water, air and whole foods) contributed to poor health in the southern part of the United States.

https://projects.fivethirtyeight.com/mortality-rates-united-states/cardiovascular/#2014

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Gender bias in treating or preventing blood clots in women

Animation of the formation of an occlusive thrombus in a vein. A few platelets attach themselves to the valve lips, constricting the opening and causing more platelets and red blood cells to aggregate and coagulate. Coagulation of unmoving blood on both sides of the blockage may propagate a clot in both directions.

A thrombus occurs when the hemostatic process, which normally occurs in response to injury, becomes activated in an uninjured or slightly injured vessel. A thrombus in a large blood vessel will decrease blood flow through that vessel (termed a mural thrombus). In a small blood vessel, blood flow may be completely cut off (termed an occlusive thrombus), resulting in death of tissue supplied by that vessel. If a thrombus dislodges and becomes free-floating, it is considered an embolus.

Some of the conditions which elevate risk of blood clots developing include atrial fibrillation (a form of cardiac arrhythmia), heart valve replacement, a recent heart attack (also known as a myocardial infarction), extended periods of inactivity (see deep venous thrombosis), and genetic or disease-related deficiencies in the blood’s clotting abilities.

Formation

Platelet activation can occur through different mechanisms such as a vessel wall breach that exposes collagen, or tissue factor encryption.[clarification needed] The platelet activation causes a cascade of further platelet activation, eventually causing the formation of the thrombus.[2]This process is regulated through thromboregulation.

Prevention and treatment

Blood clot prevention and treatment reduces the risk of stroke, heart attack and pulmonary embolism. Heparin and warfarin are often used to inhibit the formation and growth of existing thrombi; the former binds to and activates the enzyme inhibitor antithrombin III, while the latter inhibits vitamin K epoxide reductase, an enzyme needed to synthesize mature clotting factors.

Some treatments have been derived from bacteria. One drug is streptokinase, which is an enzyme secreted by several streptococcal bacteria. This drug is administered intravenously and can be used to dissolve blood clots in coronary vessels. However, streptokinase is nonspecific and can digest almost any protein, which can lead to many secondary problems. Another clot-dissolving enzyme that works faster and is more specific is called tissue plasminogen activator (tPA). This drug is made by transgenic bacteria and it converts plasminogen into the clot-dissolving enzyme plasmin.[3] There are also some anticoagulants that come from animals that work by dissolving fibrin. For example, Haementeria ghilianii, an Amazon leech, produces an enzyme called hementin from its salivary glands.[4] As of 2012, this enzyme has now been successfully produced by genetically engineered bacteria and administered to cardiac patients.

Prognosis

Thrombus formation can have one of four outcomes: propagation, embolization, dissolution, and organization and recanalization.[5]

  1. Propagation of a thrombus occurs towards the direction of the heart. This means that it is anterograde in veins or retrograde in arteries.
  2. Embolization occurs when the thrombus breaks free from the vascular wall and becomes mobile. A venous embolus (mostly from deep vein thrombosis in the lower limbs) will travel through the systemic circulation, reach the right side of the heart, and travel through the pulmonary artery resulting in a pulmonary embolism. Arterial thrombosis resulting from hypertension or atherosclerosis can become mobile and the resulting emboli can occlude any artery or arteriole downstream of the thrombus formation. This means that cerebral stroke, myocardial infarction, or any other organ can be affected.
  3. Dissolution occurs when the fibrinolytic mechanisms break up the thrombus and blood flow is restored to the vessel. This may be aided by drugs (for example after occlusion of a coronary artery). The best response to fibrinolytic drugs is within a couple of hours, before the fibrin meshwork of the thrombus has been fully developed.
  4. Organization and recanalization involves the ingrowth of smooth muscle cells, fibroblasts and endothelium into the fibrin-rich thrombus. If recanalization proceeds it provides capillary-sized channels through the thrombus for continuity of blood flow through the entire thrombus but may not restore sufficient blood flow for the metabolic needs of the downstream tissue.[citation needed]

Stroke in women

A number of factors are likely behind the surprising rise in strokes in women, including:

  • Increasing rates of obesity (women’s waists have grown by nearly two inches in the last 10 years)
  • Vitamin D3 deficiency due to lack of sun exposure. Sun avoidance also increases your risk of vitamin D sulfate deficiency, which may be an underlying cause of arterial plaque buildup (a risk factor for stroke)
  • Rising prevalence of high blood sugar levels
  • eating unprocessed, preferably organic, foods, exercising and maintaining a healthy weight will help to reduce your risk of stroke. Two additional risk factors that can have a direct impact on your stroke risk are:
    • Psychological distress. According to a 2008 study published in the journal Neurology, the more stressed you are, the greater your risk. The researchers actually found that for every notch lower a person scored on their well-being scale, their risk of stroke increased by 11 percent. Not surprisingly, the relationship between psychological distress and stroke was most pronounced when the stroke was fatal.
    • Hormone replacement therapy (HRT) and birth control pills. If you’re on one of the hormonal birth control methods (whether it’s the pill, patch, vaginal ring or implant), it is important to understand that you are taking synthetic progesterone and synthetic estrogen — something that is clearly not advantageous if you want to maintain optimal health. These contraceptives contain the same synthetic hormones as those used in hormone replacement therapy (HRT), which has well-documented risks, including an increased risk of blood clots, stroke, heart attack, and breast cancer.

Diet Soda May Dramatically Increase Your Stroke Risk

Earlier this year, research presented at the American Stroke Association’s International Stroke Conference showed that people who drink just one diet soda a day may increase their risk of stroke by 48 percent!

According to the authors:

“This study suggests that diet soda is not an optimal substitute for sugar-sweetened beverages, and may be associated with a greater risk of stroke, myocardial infarction, or vascular death than regular soda.”

While more research will likely be needed to confirm this potential link, there’s plenty of evidence showing that artificial sweeteners such as aspartame and sucralose (Splenda) can be dangerous to your health. I believe aspartame is, by far, the most dangerous artificial sweetener on the market. Reports of adverse reactions to the US FDA also support this, as aspartame accounts for over 75 percent of the adverse reactions to food additives reported to the FDA.

Embolism

An embolism is the lodging of an embolus, a blockage-causing piece of material, inside a blood vessel.[1] The embolus may be a blood clot (thrombus), a fat globule, a bubble of air or other gas (gas embolism), or foreign material. An embolism can cause partial or total blockage of blood flow in the affected vessel.[2] Such a blockage (a vascular occlusion) may affect a part of the body distant from where the embolus originated. An embolism in which the embolus is a piece of thrombus is called a thromboembolism. Thrombosis, the process of thrombus formation, often leads to thromboembolism.

An embolism is usually a pathologic event (that is, part of illness or injury). Sometimes it is created intentionally for a therapeutic reason, such as to stop bleeding or to kill a cancerous tumor by stopping its blood supply. Such therapy is called embolization.


Gender bias in treating or preventing blood clots in women

In health care, gender disparities are especially pernicious. If you are a woman, studies have shown, you are not only less likely to receive blood clot prophylaxis, but you may also receive less intensive treatment for a heart attack. If you are a woman older than 50 who is critically ill, you are at particular risk of failing to receive lifesaving interventions. If you have knee pain, you are less likely to be referred for a knee replacement than a man, and if you have heart failure, it may take longer to get EKGs.

When Dr. Elliott Haut and his team at Johns Hopkins Hospital in Baltimore designed their blood clot prevention protocol back in 2006, they didn’t expect to discover systemic gender bias. But the data were clear and the implications were alarming: Women who were trauma patients at Johns Hopkins Hospital were in considerably greater danger of dying of preventable blood clots than men.

Why? Because doctors were less likely to provide them with the appropriate blood clot prevention treatment. At Hopkins, as at many hospitals, both men and women were receiving treatment at less than perfect rates, but while 31 percent of male trauma patients were failing to get proper clot prevention, for women, the rate was 45 percent. That means women were nearly 50 percent more likely to miss out on blood clot prevention.

Blood clots, gelatinous tangles that can travel through the body and block blood flow, kill more people every year than breast cancer, AIDS and car crashes combined. But many of these clots can be avoided — if doctors prescribe the right preventive measures.

Such implicit bias, as researchers now understand, happens when we unintentionally use stereotypes or associations to make judgments. “Perhaps we take women’s symptoms less seriously, or we interpret them as having an emotional cause as opposed to a physical cause,” said Dr. Christine Kolehmainen, the associate director for women’s health at the Middleton Memorial Veterans Hospital in Madison, Wis. Studies bear this out: in one study of patients with irritable bowel syndrome, doctors were more likely to suggest that male patients receive X-rays and more likely to offer female patients tranquilizers and lifestyle advice.

In the case of blood clot prevention, doctors’ assumptions about women’s risk factors could lead to disparities in treatment. “There might be stereotypes about women’s biology or environment or occupation that could all play into medical decision-making,” Kolehmainen said.

Whether unintentional, unconscious or simply based on erroneous assumptions, treatment differentials clearly exist. Interventions like the Hopkins checklist can help correct them.


Google Women , blood clots, birth control,  pills trauma, PTSD , pregnancy

First trimester health of fetus and leukemia, Leukemia inhibitory factor

This wiki info on Leukemia inhibitory factor details when this LIF cytokine is expressed:  LIF is normally expressed in the trophectoderm of the developing embryo.

My mother’s friend is an alcoholic and birthed a daughter who had leukemia later at 20 yrs old and a son with behavioral issues. She has survived leukemia. Her son is working but always fight with her.

I urged all new mothers to lead a healthy life before and during pregnancy since all medications, alcohol and the environment affects the growing embryo. And behavioural issues also happens later in the children’s life including cancer/leukemia.

Connie


From Wiki

Leukemia inhibitory factor, or LIF, is an interleukin 6 class cytokine that affects cell growth by inhibiting differentiation. When LIF levels drop, the cells differentiate.

Function

LIF derives its name from its ability to induce the terminal differentiation of myeloid leukemic cells, thus preventing their continued growth. Other properties attributed to the cytokine include: the growth promotion and cell differentiation of different types of target cells, influence on bone metabolism, cachexia, neural development, embryogenesis and inflammation. p53 regulated LIF has been shown to facilitate implantation in the mouse model and possibly in humans.[3] It has been suggested that recombinant human LIF might help to improve the implantation rate in women with unexplained infertility.[4]

Binding/activation

LIF binds to the specific LIF receptor (LIFR-α) which forms a heterodimer with a specific subunit common to all members of that family of receptors, the GP130 signal transducing subunit. This leads to activation of the JAK/STAT (Janus kinase/signal transducer and activator of transcription) and MAPK (mitogen activated protein kinase) cascades.[5]

Expression

LIF is normally expressed in the trophectoderm of the developing embryo, with its receptor LIFR expressed throughout the inner cell mass. As embryonic stem cells are derived from the inner cell mass at the blastocyst stage, removing them from the inner cell mass also removes their source of LIF.

Pregnancy

Leukemia inhibitory factor is a cytokine expressed in the uterus during the secretory phase of the menstrual cycle, as well as expressed during a normal pregnancy.[6] Specifically, LIF is expressed in uterine endometrial glands and is under maternal control.[7]When the fertilized zygote has reached the blastocyst stage, the stromal cells surrounding the blastocyst produce leukemia inhibitory factor, which needed for the blastocyst to implant into the uterine endometrium.[6]

During pregnancy leukemia inhibitory growth factor is involved in decidualization of the maternal endometrium and implantation of the blastocyst to the endometrium.[6] LIF levels are highest on the fourth day of pregnancy indicating its involvement in implantation.[7]Implantation is critical in pregnancy in order to establish the placenta and maternal-fetal interface. Fetal endothelial cells also express the receptor for leukemia inhibitory factor, indicating it may be involved in placental angiogenesis.[8] There is also evidence leukemia inhibitory factor is involved in the survival and proliferation of primordial germ cells, which are the cellular origins of spermatozoa and oocytes.[9]

Decreased secretion of leukemia inhibitory factor is associated with poor or no implantation and, thus, pregnancy loss. Women with decreased production of LIF and other cytokines are fertile and able to become pregnant, but there is an increased risk for unexplained, recurrent miscarriages.[7][10]

Use in stem cell culture

Removal of LIF pushes stem cells toward differentiation, but they retain their proliferative potential or pluripotency. Therefore LIF is used in mouse embryonic stem cell culture. It is necessary to maintain the stem cells in an undifferentiated state, however genetic manipulation of embryonic stem cells allows for LIF independent growth, notably overexpression of the gene Nanog.

LIF is typically added to stem cell culture medium to reduce spontaneous differentiation.

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