Saturday, November 18, 2017

Dr. Greger's Superfood Bargains




Superfood Bargains


As shown in the video, the following antioxidant-rich foods are best bargains based on their antioxidant units per dollar:
  1. Purple cabbage
  2. Cinnamon 
  3. Cloves
  4. Acai
  5. Artichoke
  6. Cranberries
  7. Goji berries
  8. Apple
  9. Pecan




See Also:

  1. NutritionFacts.org
  2. Which Food Fights Cancer Better?

Saturday, October 21, 2017

Which Food Fights Cancer Better?



Below rankings are based on the food's capability to stop the proliferation of cancer cells.  So, the lower the reading is, the better it fights the cancer.

Which Vegetable Fights Cancer Better?

  1. Garlic family
  2. Brocolli family
  3. Radish
  4. Kale
  5. Yellow Onion
  6. Rutabaga
  7. Green bean
  8. Red Cabbage



Which Fruit Fights Cancer Better?

  1. Cranberry
  2. Lemon
  3. Apple
  4. Strawberry
  5. Red grape
  6. Banana
  7. Grapefruit
  8. Peach


Which Nut Fights Cancer Better?

  1. Walnut
  2. Pecan
  3. Peanut
  4. Almond
  5. Pine Nut, Cashew, Macadamia Nut
  6. Hazel Nut, Pistachio, and Brazil Nut 

Anti-Angiogenic Foods


Cancer cells are commonly present in the body, but cannot grow into tumors without hooking up a blood supply. Angiogenesis inhibitors in plant foods may help prevent this from happening.

Friday, October 20, 2017

Healthy Aging: Protein Consumption Advice for the Elderly

Protein is essential for your health. In the Mitochondrial Metabolic Therapy diet, Dr Mercola recommends you to target maximum 45 to 55 grams of protein per day for the optimal health. Why?

The reason is: when you consume more protein than your body needs, it may have the following adverse health effects:
  • Excess protein burdens kidneys with removing extra nitrogen waste products from your blood[15]
  • Excess protein stimulates the production of IGF-1 (Insulin-like growth factor one)
    • IGF-1 is a powerful stimulus of aging[12,13]
  • Excess protein stimulates mTOR
    • More details in this article
However, do consider to increase protein intake when
  • The older you get (e.g., over 65 years old) the more important protein intake becomes to avoid lean muscle loss.[12]
  • On days when you are seeking to increase your muscle mass with strentgh training
In this article, we will focus on the protein's role played in regulating mTOR's activities.



What's mTOR


mTOR is a kinase in your body. It plays a key role in the regulation of protein synthesis , cell proliferation and autophagy.[10,20] It was named as it is the mammalian Target Of Rapamycin which is an antibiotic and immune-suppressor drug that inhibits mTOR's activities.

mTOR forms two multi-protein complexes known as complex 1 (mTORC1) and 2 (mTORC2). Raptor and Rictor are the core proteins for mTORC1 and mTORC2, respectively.

In this article, we will use mTOR in general and mTORC1 in specific, but interchangeably, in the discussion of aging and carcinogenesis. Note that our understanding of the role of mTORC2 in the wider pathway is still evolving and will not be covered here.

Figure 1.  Leucine is predominantly found in animal-based food.

Regulation of Protein Synthesis


In order for cells to grow and proliferate (i.e., manufacturing more proteins), the cells must ensure that they have the resources available for protein production. For example, cells must have
  • Adequate energy resources
  • Availability of amino acid nutrients
  • Oxygen abundance
  • Proper growth factors
in order for mRNA translation to begin (i.e., protein production).

mTORC1 is known to regulate protein synthesis in the following ways:
  • When mTOR is stimulated
    • It cues the cell to grow and proliferate
    • If over-activated,
      • mTOR signaling significantly contributes to the initiation and development of tumors
      • Hence come the benefits of
        • Methionine restriction diets[21,23,27,32,38,41]
        • Leucine restrction diets (video[10,17,37]
    • When mTOR is limited
      • It instructs the cell to turn on the array of repair and maintenance processes at its disposal, including autophagy (cleaning up cellular debris), DNA repair, and activating intracellular antioxidants.
        • Autophagy and mitophagy, which are largely controlled by the mTOR, play an important role in controlling the amount of inflammation in your body and help slow down the aging process
      • Rapamycin inhibits mTORC1, and this appears to provide most of the beneficial effects of the drug
      • Plant-based diets (a better alternative) are associated with lower risk for many cancers because their capability of “down-regulation” of mTOR.

    Figure 2.  Methionine is predominantly found in animal-based food.

    mTOR and Cancer


    There is a growing body of evidence that mTORC1 is upregulated in many types of cancers and plays a role in carcinogenesis[18,19]

    Below we will discuss the relationship of mTOR and two specific cancers:

      Prostate Cancer
      • When mTOR is stimulated
        • mTORC1 is upregulated in nearly 100% of advanced human prostate cancers.[7]
      • When mTOR is limited
        • The potential prostate cancer protective effect of a plant-based diet may be explained by the reduction of dairy- and animal meat-derived leucine intake, and especially lower insulin and IGF-1 signaling of non-dairy plant-based diets attenuating overall mTORC1 activity.[10]

      Breast Cancer
      • When mTOR is stimulated 
        • Higher mTOR expression has been noted in breast cancer tumors, and associated with more aggressive disease, and lower survival rate among breast cancer patients.[8]
      • When mTOR is limited 
        • Compared with the Swedish general population, women hospitalized for anorexia nervosa—one marker of caloric restriction—prior to age 40 years had a 53% lower incidence of breast cancer; nulliparous women with anorexia nervosa had a 23% lower incidence, and parous women with anorexia nervosa had a 76% lower incidence.[9]


      How to Age Gracefully?


      Life has one imperative which is to reproduce. Once our reproductive peak has passed, nature becomes apathetic to our survival, and we commence the process of programmed degeneration we call aging. To age gracefully, the goal is to
      • Delay aging while simultaneously switch on restorative pathways — activate our internal housecleaning mechanisms (i.e., autophagy).
      As a child, milk is presented as an endocrine signaling system, which activates mTORC1 —promotes cell growth and proliferation. Naturally, milk-mediated mTORC1 signaling is restricted only to the postnatal growth phase of human.

       However, as we start aging, we should tip the balance of growth  towards more on the restorative pathways. As an adult, if you still persistently abuse the growth-promoting signaling system of cow milk. The consequences of sustained proliferative signaling is what we have witnessed today—the rising of cancer in the developed countries.

      On the other hand, plant-based diets, especially cruciferous vegetables, not only decrease leucine-dependent mTORC1 activation but also they provide natural plant-derived inhibitors of mTORC1. Increasing studies have demonstrated that
      • 3,3'-Diindolylmethane (DIM)
      • Epigallocatechin gallate (EGCG)
      • Genistein
      • Curcumin
      • Resveratrol
      • Caffeine
      all inhibit mTORC1 signaling directly or indirectly and have been suggested to reduce the risk of prostate cancers and other common cancers.

      Finally, to age gracefully, we should consdier:

      References

      1. Discovery improves understanding of cellular aging and cancer development
      2. 10 PLANT-BASED PROTEINS YOU SHOULD BE EATING
        • 1 lentils, 2 hemp seeds, 3 chia seeds 4 quinoa 5 spirulina 6 nutritional yeast 7 seeds 8 nuts 9 beans 10 tempeh/organic tofu/edamame
      3. Increasing Protein Intake After Age 65
      4. Ketogenic Diet Reduces Midlife Mortality and Improves Memory in Aging Mice
      5. X Wang, C G Proud. MTORC1 signaling: What we still don't know. J Mol Cell Biol 2011 3(4):206 – 220.
      6. J D Weber, D H Gutmann. Deconvoluting mTOR biology. Cell Cycle 2012 11(2):236 – 248.
      7. B C Melnik, S M John, P Carrera-Bastos, L Cordain. The impact of cow's milk-mediated mTORC1-signaling in the initiation and progression of prostate cancer. Nutr Metab (Lond) 2012 9(1):74.
      8. U Wazir, R F Newbold, W G Jiang, A K Sharma, K Mokbel. Prognostic and therapeutic implications of mTORC1 and Rictor expression in human breast cancer. Oncol Rep 2013 29(5):1969 – 1974.
      9. K B Michels, A Ekbom. Caloric restriction and incidence of breast cancer. Jama 2004 291(10):1226 – 1230.
      10. R F Lamb. Amino acid sensing mechanisms: An Achilles heel in cancer? FEBS J. 2012 279(15):2624 – 2631.
      11. Prevent Cancer from Going on TOR
      12. M. E. Levine et al., "Low Protein Intake Is Associated with a Major Reduction in IGF-1, Cancer, and Overall Mortality in the 65 and Younger but Not Older Population," Cell Metabolism, 19, no. 3 (2014): 407-17.
      13. Growth Hormone Receptor Deficiency Is Assoiciated With a Major Reduction in Pro-aging Signaling, Cancer and Diabetes in Humans
      14. Protein—the Good, the Bad, and the Ugly
      15. Risk Factors of Kidney Disease (Travel and Health)
      16. C H Jung, H Kim, J Ahn, T I Jeon, D H Lee, T Y Ha. Fisetin regulates obesity by targeting mTORC1 signaling. J. Nutr. Biochem. 2013 24(8):1547 – 1554.
      17. Sheen JH, Zoncu R, Kim D& Sabatini DM (2011) Defective regulation of autophagy upon leucine deprivation reveals a targetable liability of human melanoma cells in vitro and in vivo. Cancer Cell 19, 613–628.
        • Research shows that restriction of the essential amino acid leucine may provoke apoptosis in cancer cells when used in combination with inhibition of autophagy.
      18. Guertin DA and Sabatini DM: Defining the role of mTOR in cancer. Cancer Cell. 12:9–22. 2007.
      19. Xu K, Liu P, Wei W (December 2014). "mTOR signaling in tumorigenesis". Biochimica et Biophysica Acta. 1846 (2): 638–54.
      20. Toschi A, Lee E, Thompson S, et al: Phospholipase D-mTOR requirement for the Warburg effect in human cancer cells. Cancer Lett. 299:72–79. 2010.
      21. Starving Cancer with Methionine Restriction
      22. V. Agrawal, S. E. J. Alpini, E. M. Stone, E. P. Frenkel, A. E. Frankel. Targeting methionine auxotrophy in cancer: discovery & exploration. Expert Opin Biol Ther 2012 12(1):53 - 61.
      23. M. F. McCarty, J. Barroso-Aranda, F. Contreras. The low-methionine content of vegan diets may make methionine restriction feasible as a life extension strategy. Med. Hypotheses 2009 72(2):125 - 128.
      24. M. C. Ruiz, V. Ayala, M. Portero-Otín, J. R. Requena, G. Barja, R. Pamplona. Protein methionine content and MDA-lysine adducts are inversely related to maximum life span in the heart of mammals. Mech. Ageing Dev. 2005 126(10):1106 - 1114.
      25. M. López-Torres, G. Barja. Lowered methionine ingestion as responsible for the decrease in rodent mitochondrial oxidative stress in protein and dietary restriction possible implications for humans. Biochim. Biophys. Acta 2008 1780(11):1337 - 1347.
      26. E. Cohen. Chitin synthesis and degradation as targets for pesticide action. Arch. Insect Biochem. Physiol. 1993 22(1 - 2):245 - 261.
      27. P. Cavuoto, M. F. Fenech. A review of methionine dependency and the role of methionine restriction in cancer growth control and life-span extension. Cancer Treat. Rev. 2012 38(6):726 - 736.
      28. E. Boedeker, G. Friedel, T. Walles. Sniffer dogs as part of a bimodal bionic research approach to develop a lung cancer screening. Interact Cardiovasc Thorac Surg 2012 14(5):511 - 515.
      29. H. Sonoda, S. Kohnoe, T. Yamazato, Y. Satoh, G. Morizono, K. Shikata, M. Morita, A. Watanabe, M. Morita, Y. Kakeji, F. Inoue, Y. Maehara. Colorectal cancer screening with odour material by canine scent detection. Gut 2011 60(6):814 - 819.
      30. K. Yamagishi, K. Onuma, Y. Chiba, S. Yagi, S. Aoki, T. Sato, Y. Sugawara, N. Hosoya, Y. Saeki, M. Takahashi, M. Fuji, T. Ohsaka, T. Okajima, K. Akita, T. Suzuki, P. Senawongse, A. Urushiyama, K. Kawai, H. Shoun, Y. Ishii, H. Ishikawa, S. Sugiyama, M. Nakajima, M. Tsuboi, T. Yamanaka. Generation of gaseous sulfur-containing compounds in tumour tissue and suppression of gas diffusion as an antitumour treatment. Gut 2012 61(4):554 - 561.
      31. H. Y. Guo, H. Herrera, A. Groce, R. M. Hoffman. Expression of the biochemical defect of methionine dependence in fresh patient tumors in primary histoculture. Cancer Res. 1993 53(11):2479 - 2483.
      32. D. E. Epner. Can dietary methionine restriction increase the effectiveness of chemotherapy in treatment of advanced cancer? J Am Coll Nutr 2001 20(Suppl 5):443S-449S; discussion 473S-475S.
      33. E. Cellarier, X. Durando, M. P. Vasson, M. C. Farges, A. Demiden, J. C. Maurizis, J. C. Madelmont, P. Chollet. Methionine dependency and cancer treatment. Cancer Treat. Rev. 2003 29(6):489 - 499.
      34. B. C. Halpern, B. R. Clark, D. N. Hardy, R. M. Halpern, R. A. Smith. The effect of replacement of methionine by homocystine on survival of malignant and normal adult mammalian cells in culture. Proc. Natl. Acad. Sci. USA 1974 71(4):1133 - 1136.
      35. C. M. Willis, S. M. Church, C. M. Guest, W. A. Cook, N. McCarthy, A. J. Bransbury, M. R. T. Church, J. C. T. Church. Olfactory detection of human bladder cancer by dogs: Proof of principle study. BMJ 2004 329(7468):712.
      36. D. Pickel, G. P. Manucy, D. B. Walker, S. B. Hall, J. C. Walker. Evidence for canine olfactory detection of melanoma. App Anim Behav Sci 2004 89(1):107-­116.
      37. Living Longer by Reducing Leucine Intake
      38. Methionine restriction extends lifespan of Drosophila melanogaster under conditions of low amino-acid status
      39. Blattler, S. M., Cunningham, J. T., Verdeguer, F., Chim, H., Haas, W., Liu, H., Romanino, K., Ruegg, M. A., Gygi, S. P., Shi, Y. and Puigserver, P. (2012) Yin Yang 1 deficiency in skeletal muscle protects against rapamycin-induced diabetic-like symptoms through activation of insulin/IGF signaling. Cell Metab. 15, 505-517.
      40. Caloric Restriction vs. Animal Protein Restriction
      41. Methionine Restriction as a Life-Extension Strategy
      42. Heath Effects of Iron Overload and Benefits of Blood Donation (Travel to Health)
      43. Which Food Fights Cancer Better? (Travel to Health)

      Saturday, September 30, 2017

      Important Heath Effects of Dietary Fiber

      Dietary fiber consists of non-starch polysaccharides (NSP) and many other plant components such as resistant starch, resistant dextrins, inulin, lignin, chitins, pectins, beta-glucans, and oligosaccharides.

      Dietary fiber can contribute to your overall good health and longevity, and can have a positive impact on lowering risk of diseases related to Western diets, which include:[1]
      • Coronary heart disease
      • Colo-rectal cancer
      • Inflammatory bowel disease
      • Breast cancer
      • Tumor formation
      • Mineral related abnormalities
      • Disordered laxation
      • Autoimmune diseases
      by feeding and promoting healthy gut bacteria.

      In this article, we will cover the health effects of fiber from two prospectives:
      • Traditional wisdom 
        • Mostly from digestive system perspective
      • Gut Microbiota 
        • Mostly from immune system perspective


      Traditional Wisdom


      Proven benefits of dietary fiber include fewer colon polyps and thus less risk of colon cancer.  Dietary fiber is also thought to help prevent iron overload, which could promote inflammation in the colon that leads to mucosal damage, since fiber binds to iron and helps the metal pass out of the body through the digestive tract.[5]

      There are two types of dietary fiber:
      • Insoluble fiber
        • Insoluble fiber you consume is passed through your gut undigested and sweeps out it like a broom
        • Benefits
          • It is an effective laxative to relieve your constipation or irregular stools
      • Soluble fiber
        • Soluble fiber attracts fluid in your gut, creating a slow-moving gel
        • Benefits
          • It slows digestion, which allows vitamins and minerals to absorb through intestinal walls
            • For example, daily consumption of dietary fiber significantly increases calcium absorption and enhances bone mineralization during pubertal growth[11]
          • It can help lower plasma cholesterol levels and help to normalize blood glucose and insulin levels


      Gut Microbiota


      Intestinal epithelial barrier

      The total surface area of the gastrointestinal system is approximately 300 to 400 sq. m.  However, only a single epithelial layer separates you from enormous amounts of antigens of both dietary and microbial origin.

      Sitting on top of this cell lining is a layer of mucus that is also an important part of the intestinal epithelial barrier. This barrier's job is to regulate everything that passes between your intestine and the rest of your body.

      Together with the immune cells located in your gut, which represents almost 70% of the entire immune system, the barrier helps control how your immune system reacts to anything foreign. When the barrier is weak or comprised, you have a condition called leaky gut syndrome which can potentially increase your risk of autoimmune diseases.

      Short-chain fatty acids

      Dietary fiber can be fermented into short chain fatty acids (SCFAs) in your guts. SCFAs have a number of health promoting effects:[1,14]
      • Lowering the pH of the colon
      • Inhibiting growth of pathogenic organism
      • Increasing mineral absorption
      • Serving as a vital fuel source for the colonic epithelium and key regulators of immune homeostasis
        • Which serves as the prototypical example of the symbiotic nature between the microbiome and the host in terms of diet and metabolism
      Of the SCFAs, butyrate is considered to be the preferred fuel of cells of colon (i.e. colonocytes).  Without butyrates for energy, colon cells can undergo autophagy (self digestion) and die.[18]


      Beneficial gut bacteria

      Most gut bacteria reside only in the colon (which has a volume of 0.4 liters). SCFAs are produced by these beneficial colonic bacteria (probiotics) that feed on, or ferment prebiotics, which are plant products that contain adequate amounts of dietary fiber. 

      In the video above, Dr. Sonnenburg found that microbes in the guts of Americans make more enzymes that degrade mucins, compared with those in the Hadza who still lead a historic hunter-gatherer way of life in Tanzania. These enzymes allow bacteria to harvest carbohydrates from the mucosal lining of the gut, rather than from plant fiber.[20]

      In other words,
      If you’re not feeding your gut microbiome with dietary fiber,” Dr. Sonnenburg said, “your gut microbiome is literally feeding on you,” 
      which may result in changes in microbiota localization and barrier disruption in the distal gut. Interactions between resident microbes and host leading to immune dysregulation may explain several diseases that share inflammation as a common basis. 

      Besides serving as foods to colonic bacteria, scientists have also found that polyphenols bound to the fiber may have a significant physiological impact within the large intestine, affecting microflora development and intestinal antioxidant status by producing metabolites that can be absorbed through the mucosa.[13]

      Sources of Dietary Fiber 


      In recent years, it become clear that in order to be truly healthy, you need a healthy gut. Dietary fiber is used as food for your beneficial bacteria, and a healthy microbiome is essential to optimizing your health. For example, they produce compounds that help regulate your immune function and even improve brain health.

      Dietary fiber can be found from the following food sources:
      • Insoluble fiber 
        • Blackberry seeds, celery, dark-green leafy vegetables, green beans, skins of onions, and whole grains
      • Soluble fiber
        • Apples, barley, beans, berries, citrus fruits, cucumbers, oats, nuts, peas and psyllium.
      Note that many whole foods contain both soluble and insoluble fiber.  Dr. Mercola recommend consuming a minimum of 35 grams of fiber and ideally > 50 grams from whole foods per day.[12] Also, be warned that your gut may not be used to these amounts of fiber, you will want to gradually increase to those levels, as they can cause gas and bloating and even constipation until your microbiome readjusts.


      References

      1. V Kumar, A K Sinha, H P Makkar, G de Boeck, K Becker. Dietary roles of non-starch polysaccharides in human nutrition: a review. Crit Rev Food Sci Nutr. 2012;52(10):899-935
      2. How The Gut Microbiota Affects Our Health with Dr. Erica & Dr. Justin Sonnenburg
      3. Gut Bacteria Can Fluctuate With the Seasons
      4. Paleopoo: What We Can Learn from Fossilized Feces
      5. Why You Should Always Use Organic Red Onions
      6. J. I. Wurzelmann et al., "Iron Intake and the Risk of Colorectal Cancer," Cancer Epidemiology, Biomarkers and Prevention, 5, no. 7 (July 1, 1996): 503-7.  PMID: 8827353.
      7. Justin Sonnenburg on "The Good Gut"
      8. Mucins in the mucosal barrier to infection
      9. Scientists bust myth that our bodies have more bacteria than human cells
      10. Dr Greger on dietary fibers
      11. S A Abrams, I J Griffin, K M Hawthorne, L Liang, S K Gunn, G Darlington, K J Ellis. A combination of prebiotic short- and long-chain inulin-type fructans enhances calcium absorption and bone mineralization in young adolescents. Am J Clin Nutr. 2005 Aug;82(2):471-6.
      12. Fat for Fuel (Dr. Mercola)
      13. F Saura-Calixto. Concept and health-related properties of nonextractable polyphenols: the missing dietary polyphenols. J Agric Food Chem. 2012 Nov 14;60(45):11195-200.
      14. J R Goldsmith, R B Sartor. The role of diet on intestinal microbiota metabolism: downstream impacts on host immune function and health, and therapeutic implications. J Gastroenterol. 2014 May;49(5):785-98.
      15. The Good Gut: Taking Control of Your Weight, Your Mood, and Your Long-term Health
      16. Justin Sonnenburg and Erica Sonnenburg Publications
      17. Starving our microbial self: the deleterious consequences of a diet deficient in microbiota-accessible carbohydrates
      18. Donohoe, Dallas R.; Garge, Nikhil; Zhang, Xinxin; Sun, Wei; O'Connell, Thomas M.; Bunger, Maureen K.; Bultman, Scott J. (2011). "The Microbiome and Butyrate Regulate Energy Metabolism and Autophagy in the Mammalian Colon". Cell Metabolism. 13 (5): 517–26. 
      19. Lupton, Joanne R. (February 1, 2004). Microbial Degradation Products Influence Colon Cancer Risk: the Butyrate Controversy. vol. 134 no. 2: J. Nutr. pp. 479–482.
      20. Sonnenburg JL, Xu J, Leip DD, Chen CH, Westover BP, Weatherford J, Buhler JD, Gordon JI. Glycan foraging in vivo by an intestine-adapted bacterial symbiont. Science. 2005;307:1955–1959.
      21. ‘Ridiculously Healthy’ Elderly Have the Same Gut Microbiome as Healthy 30 Year-Olds
      22. Gut microbes could help trigger multiple sclerosis
      23. Constipation and Its Remedies (Travel and Health)
      24. Which Food Fights Cancer Better? (Travel to Health)

      Sunday, September 3, 2017

      "There is only time for loving" — Mark Twain



      “There isn't time, 
      so brief is life, 
      for bickerings, apologies, 
      heartburnings, callings 
      to account. There 
      is only time for loving, 
      and but an instant, 
      so to speak, for that.”

      — Mark Twain

      Saturday, September 2, 2017

      Heath Effects of Iron Overload and Benefits of Blood Donation

      Iron overload—a buildup of extra iron—without treatment can permanently damage organs such as the liver, heart, and pancreas; endocrine glands; and joints.[23] Excess Iron can also increase your risk of cancer, heart disease, and premature death.[24]


      In this article, we will cover the following topics:
      • Negative health effects of iron overload
      • Benefits of blood donation for most people


      Serum Ferritin Test


      Ferritin is a protein that stores iron and acts as a buffer against iron deficiency and iron overload. It is found in most tissues as a cytosolic protein, but small amounts are secreted into the serum where it functions as an iron carrier. Therefore, plasma ferritin is a good indirect marker of the total amount of iron stored in your body.

      The healthy range of serum ferritin lies between 20 and 80 ng/mL. Below 20, you are iron deficient, and above 80, you have an iron overload.[22]

      Health Effects of Iron Overload


      In addition to damaging your mitochondria and contributing to genetic mutations,[22] excess iron could lead to higher risk of the following:
      • Obesity
        • Iron is a growth factor
          • As low iron levels in pregnant women are associated with low birth weight babies, so are increased iron levels associated with weight gain.[16,17]
        • A large epidemiological study in Korea shows that moderately elevated levels of serum ferritin predicated future weight gain, obesity, and even severe obesity.[18]
      • Promotion of growth of pathogens
        • Excessive iron in the body facilitates growth of pathogenic bacteria, fungi, and protozoa.[19]
      • Diabetes
        • Iron is believed to influence blood glucose and insulin levels and there is a correlation between serum ferritin levels and type 2 diabetes.[13,-15]
      • Cardiovascular disease
        • A high heme iron intake, particularly in normal weight individuals, may increase the risk of stroke.[25]
        • Iron likely plays a role in heart disease by participating in the oxidation of LDL and damage of endothelial cells, both of which contribute to atherosclerosis.[11,12]
      • Neurodegenerative diseases
        • Iron is found in high concentrations in the plaques found in the brains of Alzheimer's patients and in abnormal concentrations in the brains of patients with early-onset Alzheimer's disease and Parkinson's diseases.[8-10]
      • Cancer
        • Serum ferritin is elevated in patients with many types of cancers.[4-7]
          • Excess iron could promote inflammation in the colon that leads to mucosal damage.
      • Osteoporosis
        • People with iron-loading disorders, such as hemochromatosis, are more likely to have osteoporosis.[3]

      Blood Donation


      Women in their reproductive years have an average ferritin level of 35 ng/mL, while men in the same age range have an average level of 150 ng/mL.[21] If your level of serum ferritin is above 80 ng/mL, you have an iron overload. Knowing that excess iron negatively impact your health, how can you reduce the excess?

      Your body has a limited capacity to excrete iron, so it can easily build up in and damage organs like your liver, heart, and pancreas and cause many health problems. The safest, effective, and least expensive way to remove excess iron is simply to remove blood from your body—by donating blood or getting a prescription for therapeutic phlebotomy.   For each unit of blood donated, you lose about one-quarter of a gram of iron.

      With blood donation, you also benefit from the following:
      • Multiple epidemiological studies have linked increased longevity with serum ferritin levels below a threshold of 80-90 ng/mL, which is a typical plateau for postmenopausal women.[20]
      • A randomized trial found that blood draws reduced incidence of all cancers by 37%.[7]
      • Based on a Nurses' Health Study, it shows that those who had donated blood were 50% less likely to have a stroke or heart attack.
      • Frequent blood donors have been shown to have better insulin sensitivity and a decreased risk of diabetes.[15]

      Based on the book (i.e., "Fat for Fuel") of Dr. Mercola, he recommends the following blood donation schedule dependent on your ferritin level:

      Ferritin Level
      (ng/mL)
      Donation Schedule
      (Times per Year)
      < 60Not Necessary
      100-1251 to 2
      126-2002 to 3
      201-2503 to 4
      > 2506 if possible

      References

      1. China liver problems boost demand for US blood plasma
      2. Four Unexpected Benefits of Donating Blood
      3. L. Valenti et al., "Association between Iron Overload and Osteoporosis in Patients with Hereditary Hemochromatosis," Osteoporosis International, 20, no. 4 (April, 2009): 549-55.
      4. A. A. Alkhateeb and J. R. Connor, "The Significance of Ferritin in Cancer: Anti-Oxidation, Inflammation and Tumorigenesis," Biochimica et Biophysica Acta, 1836, no. 2 (Dec 2013):245-54.
      5. J. I. Wurzelmann et al., "Iron Intake and the Risk of Colorectal Cancer," Cancer Epidemiology, Biomarkers and Prevention, 5, no. 7 (July 1, 1996): 503-7. PMID: 8827353.
      6. Y. Deugnier, "Iron and Liver Cancer," Alcohol, 30, no. 2 (2003): 145-50.
      7. L. R. Zacharski et al., "Decreased Cancer Risk after Iron Reduction in Patients with Peripheral Arterial Disease: Results from a Randomized Trial," JNCI:Journal of National Cancer Institute, 100, no. 14 (2008): 996-1002.
      8. M. A. Lovell et al., "Copper, Iron and Zinc in Alzheimer's Disease Senile Plaques," Journal of the Neurological Sciences, 158, no. 1 (June 11, 1998): 47-52.
      9. K. Jellinger et al., "Brain Iron and Ferritin in Parkinson's and Alzheimer's diseases," Journal of Neural Transmission, 2 (1990): 327.
      10. G. Bartzokis et al., "Brain Ferritin Iron as a Risk Factor for Age at Onset in Neurodegenerative Diseases," Annals of the New York Academy of Sciences, 1012, (2004): 224-36.
      11. B, J, Van Lenten et al., "Lipid-Induced Changes in Intracellular Iron Homeostasis in Vitro and in Vivo," Journal of Clinical Investigation, 95, no. 5 (1995): 2104-10.
      12. N. Stadler, R. A. Lindner, and M. J. Davies, "Direct Detection and Quantiication of Transition Metal Ions in Human Atheroslerotic Plaques: Evidence for the Presence of Elevated Levels of Iron and Coper," Arteriosclerosis, Thrombosis, and Vascular Biology, 24 (2004): 949-54.
      13. J. M. Fernandez-Real et al., "Serum Ferritin as a Component of the Insulin Resistance Syndrome," Diabetes Care, 21, no. 1 (1998): 62-68.
      14. J. Montonen et al., "Body Iron Stores and Risk of Type 2 Diabetes: Results from the European Prospective Investigation into Cancer and Nutrition (EPIC)-Potsdam Study," Diabetologia, 55, no. 10 (2012): 2613-21.
      15. J. M. Fernandez-Real, A. Lopez-Bermejo, and W. Ricart, "Iron Stores, Blood Donation, and Insulin Sensitivity and Secretion," Clinical Chemistry, 51, no. 7 (June 2005): 1201-5.
      16. D. J. Fleming et al., "Dietary Factors Associated with the Risk of High Iron Stores n the Elderly Framingham Heart Study Cohort," American Journal of Clinical Nutrition, 76, no. 6 (2002): 1375-84.
      17. T. Iwasaki et al., "Serum Ferritin Is Associated with Visceral Fat Area and Subcutaneous Fat Area," Diabetes Care, 28, no. 10 (2005): 2486-91.
      18. S. K. Park et al., "Association between Serum Ferritin Levels and the Incidence of Obesity in Korean Men: A Prospective Cohort Study," Endocrine Journal, 61, no. 3 (2014): 215-24.
      19. G. Ortiz-Estrada et al., "Iron-Saturated Lactoferrin and Pathogenic Protozoa: Could This Protein Be and Iron Source for Their Parasitic Style of Life?" Future Microbioloty, 7, no. 1 (2012): 149-64.
      20. L. Zacharski, "Ferrotoxic Disease: The Next Great Public Health Challenge," Clinical Chemistry, 60, no. 11 (November 2014): 1362-4.
      21. P. Mangan, Dumping Iron: How to Ditch This Secret Killer and Reclaim Your Health, Phalanx Press, 2016, locations 308-12.
      22. Fat for Fuel (Dr. Mercola)
      23. What is hemochromatosis?
      24. Dietary Iron Overload as a Risk Factor for HepatocellularCarcinoma in Black Africans
        • Among 24 patients, the risk of developing HCC in the iron-loaded subjects was 10.6-fold relative to individuals with normal iron status.
      25. Kaluza J, Wolk A, Larsson SC. Heme iron intake and risk of stroke: a prospective study of men. Stroke. 2013 Feb;44(2):334-9.

      Saturday, June 24, 2017

      Grand Challenges―Some of the Greatest Obstacles Facing Cancer Research Today (06/22/2017)


      Cancer Research UK on 06/22/2017 has launched the second phase of its global Grand Challenge by announcing eight new questions – identified as some of the biggest barriers to making progress against cancer – and inviting the world’s top scientists to come together with new proposals to tackle them.

      1. Devise approaches to prevent or treat cancer based on mechanisms that determine tissue specificity of some cancer genes
      2. Create novel tumour vaccinology approaches that establish or enhance successful immune responses beyond what is revealed by current checkpoint therapy
      3. Define mechanistic rules for combinatorial treatments to overcome resistance and avoid toxicity
      4. Distinguish between lethal cancers which need treating, and non-lethal cancers that don’t
      5. Identify and target tumour cells that remain dormant for many years after seemingly effective treatment
      6. Detect cancer earlier by interrogating medical and non-medical data sets using machine and deep-learning
      7. Improve treatment responses by manipulating the composition and status of the microbiota
      8. Determine the mechanisms that cause cancer without known mutagenesis, such as obesity, in order to devise novel interventions

      See Also:

      1. Understanding Cancer and Its Possible Treatments (Travel and Health)
      2. Which Food Fights Cancer Better? (Travel to Health)

      Saturday, March 18, 2017

      Hours of Sleep: How Long Is Too Little or Too Much?

      On average, adults need 7-9 hours of sleep every night to stay healthy unless you are a short sleeper (or sleepless elite).[8]  

      As a short sleeper, he/she has an easy time falling asleep and only needs four to five hours of sleep each night to feel well-rested and alert.  However, to be an elite sleeper is, for the most part, genetic and scientists estimate they make up only about 1% of the population. 

      If Sleep Too Little


      Adults who slept 5 hours or less a night had a 15% greater mortality risk compared with those sleeping 7 hours.  As we know, too little sleep may fuel insulin resistance
      • Sleep deficiency results in a higher than normal blood sugar level, which may increase your risk for diabetes[2]
      • After four nights of sleep deprivation (sleep time was only 4.5 hours per night), study participants' insulin sensitivity was 16 percent lower, while their fat cells' insulin sensitivity was 30 percent lower, and rivaled levels seen in those with diabetes or obesity[3]
      • Researchers at the University of Chicago found that losing just 3 to 4 hours of sleep over a period of several days is enough to trigger metabolic changes that are consistent with a prediabetic state.[4]


      If Sleep Too Much


      While not getting enough sleep is clearly associated with increased health risks, so is getting too much sleep. Those who slept 9 hours had a 42% increase in mortality risk.[5]

      Every person is unique. Hours of sleep needed for each is different and varies with age. See above diagram for the recommended sleep hours per your age.

      Besides hours of sleep, there are other factors to consider to get a good night sleep, read [1] for some recommendations. With a good night sleep, hopefully, you will wake up feeling energized and refreshed everyday. Stay healthy!

      References

      1. Enjoy Good Night Sleep and Live Longer (Travel and Health)
      2. Diabetes and the Night Shift Factor
      3. Impaired Insulin Signaling in Human Adipocytes After Experimental Sleep Restriction: A Randomized, Crossover Study (Annals of Internal Medicine)
      4. Knutson, K.L. Impact of sleep and sleep loss on glucose homeostasis and appetite regulation. Sleep Medicine Clinics 2007;2(2):187-97
      5. Growing Number of People Get Too Much Sleep
      6. HOW MUCH SLEEP DO WE REALLY NEED?
      7. sleep.org
      8. Here's why a 'sleepless elite' needs just 4 hours of sleep a night