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Modified Citrus Pectin


Natural Anti-Metastatic Support

Modified Citrus Pectin (MCP) is derived from pectin, a high molecular-weight polysaccharide present in the cell wall of all plants. Pectin can be pH degraded to produce a modified (smaller) polysaccharide – modified citrus pectin – which has anti-metastatic properties. MCP appears to bind with galactans on cancer cell surfaces, inhibiting aggregation and adherence to normal cells and offering anti-metastatic protection in animal models.

Modified citrus pectin is readily absorbed in the GI tract and is completely non-toxic to humans. Although there are no good studies to verify MCP’s effectiveness in humans, animal studies repeatedly demonstrate MCP’s anti-metastatic capabilities. Because of the lack of toxicity of modified citrus pectin, and because conventional medicine has no drug or treatment to prevent metastasis, I recommend taking either MCP or larch in cases of cancer to help prevent or delay metastasis.

Dose: 2-3 teaspoons, 3 times daily. This may be added to your Super Shake or other beverage.

REFERENCES

1.) Guess BW, Scholz MC,Strum SB,LamRY, Johnson HJ, Jennrich RI. Modified citrus pectin (MCP) increases the prostate-specific antigen doubling time in men with prostate cancer: a phase II pilot study.Prostate Cancer and Prostatic Diseases (2003) 6, 301–304. doi:10.1038/sj.pcan.4500679
2.) Nangia-Makker P, Hogan V, Honjo Y, et al. Inhibition of human cancer cell growth and metastasis in nude mice by oral intake of modified citrus pectin. J Natl Cancer Inst. 2002;94:1854-1862.
3.) Strum S, Scholz M, McDermed J, et al. Modified citrus pectin slows PSA doubling time: A pilot clinical trial. Presentation: International Conference on Diet and Prevention of Cancer, Tampere, Finland. May 28, 1999 – June 2, 1999.
4.) Yan J, Katz AE. PectaSol-C Modified Citrus Pectin Induces Apoptosis and Inhibition of Proliferation in Human and Mouse Androgen-Dependent and Independent Prostate Cancer Cells. Integr Cancer Ther. 2010. http://www.ncbi.nlm.nih.gov/pubmed/20462856

Macular Degeneration


Age-Related Macular Degeneration (AMD)

Age-related macular degeneration (AMD) is a disease that gradually destroys sharp, central vision. Central vision is needed for seeing objects clearly and for common daily tasks such as reading and driving. AMD affects the macula, the part of the eye that allows you to see fine detail. AMD causes no pain.

In this simulation, how a person with AMD sees the world is presented graphically. As the disease progresses the area of central vision deteriorates. The gradual destruction of light sensitive cells continues until large areas are totally lost. Peripheral vision remains, but the ability to clearly see straight ahead is gradually lost. Credit: National Eye Institute, National Institutes of Health

In some cases, AMD advances so slowly that people notice little change in their vision. In others, the disease progresses faster and may lead to a loss of vision in both eyes. AMD is a leading cause of vision loss in Americans 60 years of age and older.

Wet AMD versus dry AMD

Wet AMD occurs when abnormal blood vessels behind the retina start to grow under the macula. These new blood vessels tend to be very fragile and often leak blood and fluid. The blood and fluid raise the macula from its normal place at the back of the eye. Damage to the macula occurs rapidly.

With wet AMD, loss of central vision can occur quickly. Wet AMD is also known as advanced AMD. It does not have stages like dry AMD.

An early symptom of wet AMD is that straight lines appear wavy. If you notice this condition or other changes to your vision, contact your eye care professional at once. You need a comprehensive dilated eye exam.

Dry AMD occurs when the light-sensitive cells in the macula slowly break down, gradually blurring central vision in the affected eye. As dry AMD gets worse, you may see a blurred spot in the center of your vision. Over time, as less of the macula functions, central vision is gradually lost in the affected eye.

The most common symptom of dry AMD is slightly blurred vision. You may have difficulty recognizing faces. You may need more light for reading and other tasks. Dry AMD generally affects both eyes, but vision can be lost in one eye while the other eye seems unaffected.
 

Normal vision and the same scene as viewed by a person with age-related macular degeneration. Normal vision
Normal vision   The same scene as viewed by a person with age-related macular degeneration
The same scene as viewed by a person with age-related macular degeneration

Causes and Risk Factors

Who is at risk for AMD?

The greatest risk factor is age. Although AMD may occur during middle age, studies show that people over age 60 are clearly at greater risk than other age groups. For instance, a large study found that people in middle-age have about a 2 percent risk of getting AMD, but this risk increased to nearly 30 percent in those over age 75.

Other risk factors include:

  • Smoking. Smoking may increase the risk of AMD.
  • Obesity. Research studies suggest a link between obesity and the progression of early and intermediate stage AMD to advanced AMD.
  • Race. Whites are much more likely to lose vision from AMD than African Americans.
  • Family history. Those with immediate family members who have AMD are at a higher risk of developing the disease.
  • Gender. Women appear to be at greater risk than men.
  • Aspirin. A new study links daily aspirin use to an increased risk of macular degeneration.16

Can my lifestyle make a difference?

Diet and lifestyle can play a role in reducing your risk of developing AMD.

  • Eat a diet high in green leafy vegetables and fish.
  • Don’t smoke.
  • Avoid daily aspirin use.16

Conventional Medical Treatment for Macular Degeneration

Wet AMD can be treated with laser surgery, photodynamic therapy, and injections into the eye. None of these treatments is a cure for wet AMD. The disease and loss of vision may progress despite treatment.

  1. Laser surgery. This procedure uses a laser to destroy the fragile, leaky blood vessels. A high energy beam of light is aimed directly onto the new blood vessels and destroys them, preventing further loss of vision. However, laser treatment may also destroy some surrounding healthy tissue and some vision. Only a small percentage of people with wet AMD can be treated with laser surgery. Laser surgery is more effective if the leaky blood vessels have developed away from the fovea, the central part of the macula. (See illustration at the beginning of this document.) Laser surgery is performed in a doctor’s office or eye clinic.

    The risk of new blood vessels developing after laser treatment is high. Repeated treatments may be necessary. In some cases, vision loss may progress despite repeated treatments.

     

  2. Photodynamic therapy. A drug called verteporfin is injected into your arm. It travels throughout the body, including the new blood vessels in your eye. The drug tends to “stick” to the surface of new blood vessels. Next, a light is shined into your eye for about 90 seconds. The light activates the drug. The activated drug destroys the new blood vessels and leads to a slower rate of vision decline. Unlike laser surgery, this drug does not destroy surrounding healthy tissue. Because the drug is activated by light, you must avoid exposing your skin or eyes to direct sunlight or bright indoor light for five days after treatment.

    Photodynamic therapy is relatively painless. It takes about 20 minutes and can be performed in a doctor’s office.

    Photodynamic therapy slows the rate of vision loss. It does not stop vision loss or restore vision in eyes already damaged by advanced AMD. Treatment results often are temporary. You may need to be treated again.

     

  3. Injections. Wet AMD can now be treated with new drugs that are injected into the eye (anti-VEGF therapy). Abnormally high levels of a specific growth factor occur in eyes with wet AMD and promote the growth of abnormal new blood vessels. This drug treatment blocks the effects of the growth factor.

    You will need multiple injections that may be given as often as monthly. The eye is numbed before each injection. After the injection, you will remain in the doctor’s office for a while and your eye will be monitored. This drug treatment can help slow down vision loss from AMD and in some cases improve sight.

Nutritional Treatment of Age-Related Eye Disease Study (AREDS)

Age-Related Eye Disease Study (AREDS)

The National Eye Institute’s Age-Related Eye Disease Study (AREDS) found that taking a specific high-dose formulation of antioxidants and zinc reduces the risk of advanced AMD and its associated vision loss by 25%, slowing AMD’s progression from the intermediate stage to the advanced stage.

 The specific daily amounts of antioxidants and zinc used by the study researchers were 500 milligrams of vitamin C, 400 International Units of vitamin E, 15 milligrams of beta-carotene (often labeled as equivalent to 25,000 International Units of vitamin A), 80 milligrams of zinc as zinc oxide, and two milligrams of copper as cupric oxide. Copper was added to the AREDS formulation containing zinc to prevent copper deficiency anemia, a condition associated with high levels of zinc intake.

Can diet alone provide the same high levels of antioxidants and zinc as the AREDS formulation?

No. The high levels of vitamins and minerals are difficult to achieve from diet alone. However, previous studies have suggested that people who have diets rich in green leafy vegetables have a lower risk of developing AMD.

Can a daily multivitamin alone provide the same high levels of antioxidants and zinc as the AREDS formulation?

No. The formulation’s levels of antioxidants and zinc are considerably higher than the amounts in any daily multivitamin.

If you are already taking daily multivitamins and your doctor suggests you take the high-dose AREDS formulation, be sure to review all your vitamin supplements with your doctor before you begin. Because multivitamins contain many important vitamins not found in the AREDS formulation, you may want to take a multivitamin along with the AREDS formulation. For example, people with osteoporosis need to be particularly concerned about taking vitamin D, which is not in the AREDS formulation. 1

How to Make Vision Supplements Work Better

Many people who take the AERDS nutritional supplement formula do not benefit from it and the disease progresses. Only about 25% of study participants benefited. Also note that this formula often slows the advancement of the disease. Just because you don’t notice improvement doesn’t mean it isn’t working.

Some holistic physicians, myself included, have found that poor assimilation — especially a decrease of gastric acid function in the stomach — is an important factor in the development of AMD. No matter how many supplements one takes, if they are not assimilated, they are of no value.

It is probably no coincidence that the risk of AMD increases with age and so does the decline of stomach acid production. Contrary to popular belief, most people who experience “heartburn” actually have too little stomach acid, not too much. Find out how that happens in this article: What’s Burning You?

So, in addition to taking eye nutrients, improving digestion and assimilation is also highly recommended.

Dr. Myatt’s Recommendations for Macular Degeneration

  1. Diet: eat a diet high in antioxidant nutrients (especially green vegetables), high in Omega-3 fatty acids (from fish) and low in Omega-6 fatty acids.
  2. Gastric function: Perform a Gastric Acid Self-Test or ask your holistic physician to perform a Heidleberg gastric analysis. Make corrections to gastric acid function as indicated by the test.
  3. Vision supplements: The following are specifically recommended for macular degeneration:

    I) Maxi Multi– optimal potency multiple vitamin / mineral / trace mineral supplement. 3 caps, 3 times per day with meals.

    Vision was the same or better in 88% of people with AMD who took a multiple vitamin / mineral supplement compared with 59% of those who those who did not take the supplement. This is a statistically significant difference. The supplement used in this study contained beta-carotene, vitamin C, vitamin E, zinc, copper, manganese, selenium, and riboflavin. 2  Other studies have confirmed the importance of vitamins A, C, E, zinc and other nutrients found in a quality multiple vitamin/ mineral formula. 3,5 More recent studies have also shown the importance of B complex vitamins in AMD.4

    II.) Maxi Marine O-3: (high potency fish oil). 1 cap, 2 times per day. A diet high in omega-3 fatty acids, especially from fish oil, has been associated with lower risk of macular degeneration in multiple studies. 5-10

    III.)  Lutein Plus (lutein and zeaxanthin).  1 cap, 1-2 times per day with meals. Lutein and zeaxanthin are two carotenoids that act directly in the macula to protect it from damaging effects of excess light.  Along with vitamins C and E, they are part of the antioxidant defense system of the macula.11      

    Studies have shown that lutein and zeaxanthin reduce the risk of AMD and may slow progression. 3-5, 11-14
    Smokers have an increased need for these carotenoids. 14      

How Long to See Results?

One study suggests that it takes at least 6 months of supplementation to see results. 15
 

References

  1. www.nei.nih.gov
  2. Olson RJ. Supplemental dietary antioxidant vitamins and minerals in patients with macular degeneration. J Am Coll Nutr 1991;10:550.
  3. Krishnadev N, Meleth AD, Chew EY. Nutritional supplements for age-related macular degeneration. Curr Opin Ophthalmol. 2010 May;21(3):184-9.
  4. Olson JH, Erie JC, Bakri SJ. Nutritional supplementation and age-related macular degeneration. Semin Ophthalmol. 2011 May; 26(3):131-6.
  5. Ho L, van Leeuwen R, Witteman JC, van Duijn CM, Uitterlinden AG, Hofman A, de Jong PT, Vingerling JR, Klaver CC. Reducing the genetic risk of age-related macular degeneration with dietary antioxidants, zinc, and ω-3 fatty acids: the Rotterdam study. Arch Ophthalmol. 2011 Jun;129(6):758-66.
  6. Mance TC, Kovacević D, Alpeza-Dunato Z, Stroligo MN, Brumini G. The role of omega 6 to omega 3 ratio in development and progression of age-related macular degeneration.Coll Antropol. 2011 Sep;35 Suppl 2:307-10.
  7. Merle B, Delyfer MN, Korobelnik JF, Rougier MB, Colin J, Malet F, Féart C, Le Goff M, Dartigues JF, Barberger-Gateau P, Delcourt C. Dietary omega-3 fatty acids and the risk for age-related maculopathy: the Alienor Study. Invest Ophthalmol Vis Sci. 2011 Jul 29;52(8):6004-11. Print 2011 Jul.
  8. Sangiovanni JP, Agrón E, Meleth AD, Reed GF, Sperduto RD, Clemons TE, Chew EY; Age-Related Eye Disease Study Research Group. {omega}-3 Long-chain polyunsaturated fatty acid intake and 12-y incidence of neovascular age-related macular degeneration and central geographic atrophy: AREDS report 30, a prospective cohort study from the Age-Related Eye Disease Study. Am J Clin Nutr. 2009 Dec;90(6):1601-7. Epub 2009 Oct 7.
  9. SanGiovanni JP, Chew EY, Agrón E, Clemons TE, Ferris FL 3rd, Gensler G, Lindblad AS, Milton RC, Seddon JM, Klein R, Sperduto RD; Age-Related Eye Disease Study Research Group. The relationship of dietary omega-3 long-chain polyunsaturated fatty acid intake with incident age-related macular degeneration: AREDS report no. 23. Arch Ophthalmol. 2008 Sep;126(9):1274-9.
  10. Seddon JM, Rosner B, Sperduto RD, Yannuzzi L, Haller JA, Blair NP, Willett W. Dietary fat and risk for advanced age-related macular degeneration. Arch Ophthalmol. 2001 Aug;119(8):1191-9.
  11. Fletcher AE. Free radicals, antioxidants and eye diseases: evidence from epidemiological studies on cataract and age-related macular degeneration. Ophthalmic Res. 2010;44(3):191-8. Epub 2010 Sep 9.
  12. SanGiovanni JP, Chew EY, Clemons TE, Ferris FL 3rd, Gensler G, Lindblad AS, Milton RC, Seddon JM, Sperduto RD. The relationship of dietary carotenoid and vitamin A, E, and C intake with age-related macular degeneration in a case-control study: AREDS Report No. 22.  Arch Ophthalmol. 2007 Sep;125(9):1225-32.
  13. Tan JS, Wang JJ, Flood V, Rochtchina E, Smith W, Mitchell P. Dietary antioxidants and the long-term incidence of age-related macular degeneration: the Blue Mountains Eye Study.Ophthalmology. 2008 Feb;115(2):334-41. Epub 2007 Jul 30.
  14. Schweigert FJ, Reimann J. [Micronutrients and their relevance for the eye–function of lutein, zeaxanthin and omega-3 fatty acids]. Klin Monbl Augenheilkd. 2011 Jun;228(6):537-43. Epub 2010 Aug 25.
  15. Cangemi FE. TOZAL Study: an open case control study of an oral antioxidant and omega-3 supplement for dry AMD. BMC Ophthalmol. 2007 Feb 26;7:3.
  16. Paulus T.V.M. de Jong, Usha Chakravarthy, Mati Rahu, Johan Seland, Gisele Soubrane, Fotis Topouzis, Johannes R. Vingerling, Jesus Vioque, Ian Young, Astrid E. Fletcher. Associations between Aspirin Use and Aging Macula Disorder:The European Eye Study. Ophthalmology Volume 119, Issue 1 , Pages 112-118, January 2012

 

Turmeric:


Powerful Cancer-fighting Herb
that drug companies are rushing to imitate.

An ever-growing body of scientific evidence demonstrates that turmeric — the bright yellow spice herb used in East Indian cooking — has potent anti-cancer properties. According to Bharat Aggarwal, chief of cytokine research at the University of Texas M.D. Anderson Cancer Center, the research to date shows that turmeric’s anti-cancer “promise is enormous.” This evidence and opinion was reported at the recent Society for Integrative Oncology conference and is also posted on the American Cancer Society’s website (www.cancer.org).

Turmeric, and it’s primary active ingredient curcumin, is the main ingredient in curry and a member of the ginger family. In addition to it’s anti-cancer properties, turmeric is a potent antioxidant, anti-inflammatory and liver-protecting herb. Expect to see and read a lot more about this herb in the future, although Wellness Club members have known about the benefits of turmeric for over a decade!

You can learn more about turmeric and find one of the most potent turmeric supplements available on The Wellness Club website by visiting Turmeric: Antioxidant, Anti-inflammatory and Anti-Cancer Herb.

References

1.) Curcumin inhibits the mammalian target of rapamycin-mediated signaling pathways in cancer cells. Beevers,Li,Liu,Huang. Int J Cancer. 2006 Mar 20
2.) Antitumor action of curcumin in human papillomavirus associated cells involves downregulation of viral oncogenes, prevention of NFkB and AP-1 translocation, and modulation of apoptosis. Divya CS, Pillai MR. Mol Carcinog. 2006 May;45(5):320-32.
3.) Curcumin mediates ceramide generation via the de novo pathway in colon cancer cells. Moussavi M, Assi K, Gomez-Munoz A, Salh B. Carcinogenesis. 2006 Feb 25; [Epub ahead of print]
4.) Overexpression of p65/RelA potentiates curcumin-induced apoptosis in HCT116 human colon cancer cells. Collett GP, Campbell FC. Carcinogenesis. 2006 Feb 23; [Epub ahead of print]
5.) Induction of G2/M arrest and inhibition of cyclooxygenase-2 activity by curcumin in human bladder cancer T24 cells. Park C, Kim GY, Kim GD, Choi BT, Park YM, Choi YH. Oncol Rep. 2006 May;15(5):1225-31.
6.) Molecular targets of dietary agents for prevention and therapy of cancer. Aggarwal BB, Shishodia S. Biochem Pharmacol. 2006 Feb 23; [Epub ahead of print]
7.) Inhibition of telomerase activity and induction of apoptosis by curcumin in K-562 cells. Chakraborty S, Ghosh U, Bhattacharyya NP, Bhattacharya RK, Roy M. Mutat Res. 2006 Jan 27; [Epub ahead of print]
8.) Curcumin differentially sensitizes malignant glioma cells to TRAIL/Apo2L-mediated apoptosis through activation of procaspases and release of cytochrome c from mitochondria. Gao X, Deeb D, Jiang H, Liu YB, Dulchavsky SA, Gautam SC. J Exp Ther Oncol. 2005;5(1):39-48.
9.) Multiple biological activities of curcumin: a short review. Maheshwari RK, Singh AK, Gaddipati J, Srimal RC. Life Sci. 2006 Mar 27;78(18):2081-7. Epub 2006 Jan 18.
10.) Curcumin, an atoxic antioxidant and natural NFkappaB, cyclooxygenase-2, lipooxygenase, and inducible nitric oxide synthase inhibitor: a shield against acute and chronic diseases. Bengmark S. JPEN J Parenter Enteral Nutr. 2006 Jan-Feb;30(1):45-51.
11.) Antiproliferation and apoptosis induced by curcumin in human ovarian cancer cells. Shi M, Cai Q, Yao L, Mao Y, Ming Y, Ouyang G. Cell Biol Int. 2006 Mar;30(3):221-6. Epub 2005 Dec 22.
12.) Synergistic inhibitory effects of curcumin and 5-fluorouracil on the growth of the human colon cancer cell line HT-29. Du B, Jiang L, Xia Q, Zhong L. Chemotherapy. 2006;52(1):23-8. Epub 2005 Dec 9.
13.) Curcumin induces human HT-29 colon adenocarcinoma cell apoptosis by activating p53 and regulating apoptosis-related protein expression. Song G, Mao YB, Cai QF, Yao LM, Ouyang GL, Bao SD. Braz J Med Biol Res. 2005 Dec;38(12):1791-8. Epub 2005 Nov 9.
14.) Inhibition of cellular proliferation and induction of apoptosis by curcumin in human malignant astrocytoma cell lines. Nagai S, Kurimoto M, Washiyama K, Hirashima Y, Kumanishi T, Endo S. J Neurooncol. 2005 Sep;74(2):105-11.
15.) Curcumin inhibits human colon cancer cell growth by suppressing gene expression of epidermal growth factor receptor through reducing the activity of the transcription factor Egr-1. Chen A, Xu J, Johnson AC. Oncogene. 2006 Jan 12;25(2):278-87.

 

 

Argyria

A Bluish Discoloration Of Tissues (esp. Skin) Due To Silver

Regarding reports of silver turning skin blue in humans:

It is certainly possible to over-ingest silver-containing solutions abd cause a permanant bluish discoloration of skin and other tissues. To achieve this effect requires massive ingestion of silver far in excess of anything therapeutic or sensible.

The following information comes from Wikipedia:

A prominent case was that of Stan Jones of Montana, a Libertarian candidate for the United States Senate in 2002 and 2006. Jones acquired argyria through consumption of a home-made silver product that he made due to fears that the Year 2000 problem would make antibiotics unavailable. The peculiar colouration of his skin was featured prominently in media coverage of his unsuccessful campaign, though Jones contends that the best-known photo was “doctored”. Jones promised that he was not using his silvery complexion as a gimmick. He continues to promote the use of colloidal silver as a home remedy. He has said that his good health, minus the unusual skin tone, is the result of his use of colloidal silver.

On December 20, 2007 the world press published stories about Paul Karason, a California man whose entire skin gradually turned blue after consuming colloidal silver made by himself with distilled water, salt and silver, and using a silver salve on his face in an attempt to treat problems with his sinus, dermatitis, acid reflux, and other issues. This happened because he drank gallons of colloidal silver per week for years.

In our opinion, neither of the cases cited above represents sensible or prudent use of colloidal silver – in fact there is ample evidence that the home-made soludions used by these two persons are not in fact true colloidal suspensions!

Silver has a long and honorable history of use in human healing. There is ample literature attesting to it’s safety and efficacy. Here is an abstract from just one article:

Silver has a long and intriguing history as an antibiotic in human health care. It has been developed for use in water purification, wound care, bone prostheses, reconstructive orthopaedic surgery, cardiac devices, catheters and surgical appliances. Advancing biotechnology has enabled incorporation of ionizable silver into fabrics for clinical use to reduce the risk of nosocomial infections and for personal hygiene. The antimicrobial action of silver or silver compounds is proportional to the bioactive silver ion (Ag(+)) released and its availability to interact with bacterial or fungal cell membranes. Silver metal and inorganic silver compounds ionize in the presence of water, body fluids or tissue exudates. The silver ion is biologically active and readily interacts with proteins, amino acid residues, free anions and receptors on mammalian and eukaryotic cell membranes. Bacterial (and probably fungal) sensitivity to silver is genetically determined and relates to the levels of intracellular silver uptake and its ability to interact and irreversibly denature key enzyme systems. Silver exhibits low toxicity in the human body, and minimal risk is expected due to clinical exposure by inhalation, ingestion, dermal application or through the urological or haematogenous route. Chronic ingestion or inhalation of silver preparations (especially colloidal silver) can lead to deposition of silver metal/silver sulphide particles in the skin (argyria), eye (argyrosis) and other organs. These are not life-threatening conditions but cosmetically undesirable. Silver is absorbed into the human body and enters the systemic circulation as a protein complex to be eliminated by the liver and kidneys. Silver metabolism is modulated by induction and binding to metallothioneins. This complex mitigates the cellular toxicity of silver and contributes to tissue repair. Silver allergy is a known contra-indication for using silver in medical devices or antibiotic textiles.

Reference

Lansdown AB (2006). “Silver in health care: antimicrobial effects and safety in use”. Current Problems in Dermatology 33: 17–34. http://www.ncbi.nlm.nih.gov/pubmed/16766878

Longevity Lab Profile

Dr. Myatt’s Longevity Lab Profile

Americans LOVE medical tests. This isn’t just my professional opinion after twenty–three years in practice, it has been proven. In fact, we spend more on medical testing than any other country in the world

In spite of all the “looking” and testing, the average American lifespan is 78 years, 11 years behind the longest-lived industrial nation and 51st in the world.(33) All our testing isn’t helping us live longer or even better. Much of this testing is a bust.

So, am I recommending that we forgo ALL medical testing? Heck no! A simple chemistry screen and CBC (complete blood count) annually can tell us a lot about one’s general state of health and help us make early “course changes” to avoid problem. I always recommend these simple tests annually. They are inexpensive and easy, “cheap health insurance” in my opinion. I get mine done twice per year.

However, in examining the scientific literature and looking for the most important markers to follow, there are several tests that emerge as being true “longevity markers.” These tests have an “optimal range” that is smaller (tighter) than the conventional medical range. Stay within that range, and your risk of “all cause mortality” is dramatically diminished.

SO, on that note, I present the simple collection of tests that I consider an indispensable part of an anti-aging / longevity program.

1.) hgA1C optimal range: 5.0-5.4

Hemoglobin A1C is a measure of the amount of hemoglobin’s exposure to plasma glucose. It is now considered the “Gold Standard” for monitoring blood sugar levels because it reflects what the average blood sugar levels have been for the preceding three months or so.

Conventional reference ranges are typically 4.0-5.6, with 5.6-6.4 considered “pre diabetes.” However, one large study found that an hgA1C outside the 5.0-5.4 range was associated with an increased risk of death from all causes. This is called “all cause mortality.” (1)

2.) TSH optimal: 0.5-1.4 (check thyroid hormones below 0.5 to evaluate for hyperthyroid)

Thyroid Stimulating Hormone is a measure of the amount of TSH that is being put out by the pituitary gland in order to stimlate thyroid hormone output. In conventional medicine, it is considered the “Gold Standard” screen test for thyroid function.

I have actually seen many patients with abnormal thyroid hormone levels (free T3 and free T4) who had normal TSH levels. I have also seen patients with abnormal TSH levels who had normal thyroid hormone levels. This makes me question TSH’s “Gold Standard” position as the best screen for thyroid hormones. I personally prefer to also test the thyroid hormones directly the first time I evaluate thyroid function. I also look at “reverse T3” which can block thyroid utilization even in the presence of normal thyroid levels. But, I digress.

The standard “normal” range for TSH on lab tests is about 0.5 to 4.6 mIU/L. This range reflects two standard deviations around the US mean, meaning that 95% of the population falls in the “normal” range. Unfortunately, there is no evidence that TSH values in this range are health or normal.  In fact, many people with “normal” TSH live with symptoms of hypothyroidism.

Research demonstrating that many people are thyroid-deficient and that improving thyroid status can dramatically improve health has been conducted in Europe:

The HUNT study of 25,000 healthy Norwegians found that those with a TSH level of 1.5 to 2.4 were 41% more likely to die over the next 8 years than those with TSH below 1.5; those with TSH 2.5-3.4 were 69% more likely to die.(2)

3.) hs-CRP (highly sensitive C-reactive protein). Optimal range <1.3.

Inflammation is recognized as an important mechanism of cardiovascular injury. Subtle inflammation as measured by hs-CRP, is highly associated with heart disease risk and with an increased risk of death from all causes. (3-19)

It should be noted that hs-CRP was an “emerging risk factor” back in 1998 when I first reported on it in HealthBeat. Many physicians had not even heard of the test, including cardiologists. I advised my patients to get the test even though it wasn’t yet covered by insurance. Today, ordering an hs-CRP is “standard of care” and a routine part of most conventional cardiac risk profiles. But it should also be a routine anti-aging marker since it is associated with all-cause mortality.

4.) Ferritin optimal range 25-80; slightly < 50 may be ideal.

Ferritin is an iron storage protein and is a measure of  body iron stores. High (even “high normal”) iron levels increase free radical production and are highly associated with increased risk of atherosclerosis and peripheral vascular disease. Serum ferritin was one of the strongest risk predictors of overall progression of atherosclerosis. (20-29)

5.) Vitamin D (optimal range: 50-60 nmol/liter)

There is a strong association between vitamin D levels and all-cause mortality. All-cause mortality was 26% higher among those in the lowest vitamin D quartile compared with those in the highest quartile with optimal vitamin D status above 32.1 ng/mL after controlling for baseline demographics. (30-32)

This Panel INCLUDES all tests of the Opti-Plus Profile

N402 – Longevity Lab Profile – 273.00

Enter Quantity Desired and Click “Add To Cart” Button

References

  1. Carson AP, Fox CS, McGuire DK, Levitan EB, Laclaustra M, Mann DM, Muntner P.Carson AP, Fox CS, McGuire DK, Levitan EB, Laclaustra M, Mann DM, Muntner P. Low hemoglobin A1c and risk of all-cause mortality among US adults without diabetes. Circ Cardiovasc Qual Outcomes. 2010 Nov;3(6):661-7. doi: 10.1161/CIRCOUTCOMES.110.957936. Epub 2010 Oct 5.
  2. Asvold BO et al. Thyrotropin levels and risk of fatal coronary heart disease: the HUNT study. Arch Intern Med. 2008 Apr 28;168(8):855-60. http://pmid.us/18443261.
  3. Yeh ET. High-sensitivity C-reactive protein as a risk assessment tool for cardiovascular disease.Clin Cardiol. 2005 Sep;28(9):408-12.
  4. Paoletti R, Bolego C, Poli A, Cignarella A. Metabolic syndrome, inflammation and atherosclerosis. Vasc Health Risk Manag. 2006;2(2):145-52.
  5. Comparison of C-reactive protein and low-density lipoprotein cholesterol levels in the prediction of first Cardiovascular events. N Engl J Med. 2002 Nov 14;347(20):1557-65.
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