Dr Paul Clayton 2013<\/p>\n
Sarcopenia \u2013 loss of muscle mass \u2013 is a very common but surprisingly little-known
\ncondition related to bad nutrition and an inactive lifestyle.<\/p>\n
From early middle age on, most of us lose muscle mass. It\u2019s not inevitable \u2013 a very
\nphysically active lifestyle can delay or prevent it \u2013 but people who are physically inactive lose
\nup to 5% of their muscle mass per decade from age 30! Some estimates are as high as 1% a
\nyear. As the urban lifestyle tends to be very inactive, this age-related loss of muscle mass
\n(sarcopenia) affects very large numbers of people: over 20% of 60 to 70 year-olds, rising
\nto 50% of the over 75s.<\/p>\n
And as numbers of elderly folk increase, the socio-economic costs of ill health caused by
\nsarcopenia have become very significant. The most recent (2004) survey of US costs put
\nthem as high as $26 billion a year(1) and in 2008 the Centres for Disease Control named
\nsarcopenia as one of the top five health risks facing the US population. The EU has adopted
\na similar position.<\/p>\n
Patients whose lifestyles have left them with sarcopenia generally also have symptoms of a
\nnumber of related medical conditions. When the loss of muscle mass has led to a loss of
\nmobility and appetite, osteoporosis and general wasting often co-present as the so-called
\n\u2018frailty syndrome\u2019. If calorie intake has been preserved, sarcopenia generally presents with
\nobesity (\u2018sarcobesity\u2019) and with diabetes (\u2018metobesity\u2019).<\/p>\n
Not just an issue of fracture risk<\/strong> Muscle is an important metabolic organ <\/strong> If muscle mass has fallen, the capacity of muscle to take up and \u2018burn\u2019 glucose is Causes of sarcopenia<\/strong> .. Endocrine shift<\/em>: the menopause and viropause or andropause trigger hormone shifts .. Sedentary lifestyle<\/em>: a risk factor for sarcopenia and many other disorders.(3) Being .. Chronic inflammation<\/em>: a vicious cycle, whereby chronic inflammation drives muscle breakdown and the build-up of fat drives further inflammation.<\/p>\n .. Dysnutrition<\/em>(4): insufficient protein and the co-factors required to build muscle protein. .. Smoking<\/em>: worsens chronic inflammation<\/p>\n Countering the risk factors<\/strong> When fully implemented, this strategy triggers an energy switch called AMP-Kinase (AMP-K) If the combination of exercise and optimum nutrition were integrated into a pill, it would be The supplement industry is selling high protein shakes and other foods for sarcopenia, with Exercise doesn\u2019t have to mean pumping iron<\/strong> Aerobic exercise lowers levels of oxygen (and cAMP) in muscle, and this is one way of Exercise Chinese-style?<\/strong> Anaerobic and isometric exercise can be as effective as the traditional aerobic and Initial studies showed that Jiaogulan extracts activated AMP-K. Later work proved that the More research showed that the standardised extract produced all the metabolic benefits of So is this supplement a weight loss product? Yes and no. It has traditionally been used to The spectrum of effects of Jiaogulan will undoubtedly give it an invaluable role in the The standardised extract will be available in 2014 (Jiaogulan teas are already around) and REFERENCES<\/p>\n 1. Janssen I, Shepard DS, Katzmarzyk PT, Roubenoff R The healthcare costs of sarcopenia in the United States. J Am Geriatr Soc. 2004 Jan;52(1):80-5.
\nThis explains why sarcopenia is not only associated with the falls that cause fractures,
\nbut also with all the complications of diabetes including a raised risk of vascular disease,
\nheart attacks, strokes, blindness, liver and kidney disease and a range of gastrointestinal
\ncancers. In short, sarcopenia contributes to the entire ageing process and in the process inflicts
\na substantial burden of morbidity and mortality.(2)<\/p>\n
\nSarcopenia is at the centre of all these diseases because muscle is not just a way of moving our
\nbodies; it is also a highly important metabolic organ, and is critically involved in blood
\nglucose control and plasma lipid (blood fat) profiles. When we consume carbohydrates, for
\nexample, and insulin kicks in, some glucose istaken up by the liver and stored as glycogen \u2013
\nbut in a fit and physically active person, the bulk of blood glucose is taken up and used as
\nfuel in the skeletal muscles.<\/p>\n
\ndramatically compromised. This contributes to insulin resistance, glycative stress (where sugar
\nmolecules bind to protein in the body), chronic inflammation, widespread tissue damage and
\naccelerated ageing. Similarly, loss of muscle bulk and functionality impairs the muscles\u2019
\nability to remove LDL cholesterol from the circulation \u2013 creating an situation where the
\ndanger of atheroma (hardening and furring of the arteries) is heightened.<\/p>\n
\nBy examining the causes of sarcopenia we can begin to design programmes that will delay or
\neven prevent this core element of the ageing process. This will improve quality of life as we
\nage, increase the independence of the elderly, reduce their needs for health care and cut
\nhealthcare costs. The causes include:<\/p>\n
\nthat degrade muscle in women and men<\/p>\n
\nbed-bound is even worse; if a relatively healthy person in their 70s is bed-bound for 10 days, they can lose 10 percent of their total lean leg mass.<\/p>\n
\nFast foods\u2014foods cooked at high temperatures contain high levels of pro-inflammatory compounds.<\/p>\n
\nRemoving or countering the above risk factors is the key to reducing the incidence and
\nseverity of sarcopenia, and all the related pathologies. The optimal protective strategy
\nincludes exercise, enhanced nutrition and of course smoking cessation.<\/p>\n
\nand creates a favourable environment in which the body can start to burn more energy as fuel
\nfor movement and to stop storing it as fat and cholesterol. [See refs 5-9 for AMP-K mode of action.]<\/p>\n
\nregarded as a wonder drug \u2013 perhaps the wonder drug of our age. It replaces two of the
\nmost lucrative pharmaceutical drug sectors (anti-glycemic agents and statins), providing
\ngreater benefits than both of them without any of the adverse effects.<\/p>\n
\nlimited success. There is little point in pouring amino acids into the body if it is suffering from
\nchronic inflammation, and if the muscles are not being \u2018instructed\u2019 to grow. It is essential to
\nput out the fires first, which easily can be achieved with a comprehensive anti-
\ninflammatory regime as outlined in my recent e-book Inflamm-ageing. It is slightly more
\ndifficult to generate the muscle growth signals.<\/p>\n
\nThe most familiar way of growing and strengthening muscle is via exercise, but many
\nelderly people are not willing to exercise to the level needed, and for those with disability or
\ndisease this may be impossible. Luckily, it is not necessary to run marathons or to pump
\niron. These classical forms of exercise are aerobic and isotonic (ie you gasp for breath and
\nmove your limbs), but we now know that equal gains can be made via anaerobic and isometric
\nexercise, where you do not become breathless and indeed hardly have to move.<\/p>\n
\nactivating the AMP-K enzyme. However, the latest research shows that AMP-K can also be
\nactivated by putting tension on muscle fibres, and this can be achieved in practical terms by
\nany form of resistance exercise, which can even be semi-passive eg. standing on a
\nvibrating plate(10). But if even this is too much, work is well advanced on a supplement \u2026<\/p>\n
\nEthno-botanical screening in South Korea, identified the herb Gymnestemma pentaphyllum
\nas a candidate for research. Traditionally made into a tonic to revitalise the frail and elderly, its
\npopularity and its Chinese name Jiaogulan (\u2018little herb of immortality\u2019) sparked the
\nresearchers\u2019 interest.<\/p>\n
\nisotonic forms.<\/p>\n
\nsaponins Damulin A and B were the actives\u2014very active in fact, far more so than
\nthe synthetic compound AICAR that activates AMP-K so effectively that it is thought to
\nhave won the Tour de France in 2009 and 2010 (before it was banned!).<\/p>\n
\nexercise; including improved insulin sensitivity and improved blood fat (plasma
\nlipid) profiles and fat loss, in both pre-clinical models(11) and an initial clinical trial(12) recently published in the prestigious journal Obesity, reflecting the robust nature of the study. The
\nfat loss was preferentially from the hard-toshift visceral fat depots \u2013 exactly the same
\nones that are targeted by exercise.<\/p>\n
\nimprove blood glucose control and plasma lipid profiles. It has a role in sport and is useful
\nin improving muscle fitness and restoring insulin sensitivity not only in sedentary types
\nbut also in those with disabilities which make physical activity difficult or impossible.<\/p>\n
\nmanagement of sarcopenia through its ability to activate AMP-K, combined with its anti-
\ninflammatory effect and its down-regulation of MTOR (which slows muscle wasting).<\/p>\n
\ngreat things are expected. I believe this type of supplementation could save \u00a34 billion in
\nthe UK alone if widely implemented.(13)<\/p>\n
\n2. Parr EB, Coffey VG, Hawley JA. ‘Sarcobesity’: a metabolic conundrum. Maturitas. 2013 Feb;74(2):109-13.
\n3. Owen N, Sparling PB, Healy GN, Dunstan DW, Matthews CE. Sedentary behavior: emerging evidence for a new health risk. Mayo Clin Proc. 2010 Dec;85(12):1138-41.
\n4. Vandewoude MF, Alish CJ, Sauer AC, Hegazi RAJ. Malnutritionsarcopenia syndrome: is this the future of nutrition screening and assessment for older adults? Aging Res. 2012; 2012:651570.
\n5. Chen MB, Zhang Y, Wei MX, Shen W, Wu XY, Yao C, Lu PH. Activation of AMP-activated protein kinase (AMPK) mediates plumbagin-induced apoptosis and growth inhibition in cultured human colon cancer cells. Cell Signal. 2013 May 25.
\n6. Yang X, Huang N. Berberine induces selective apoptosis through the AMPK-\u001fmediated mitochondrial\/caspase pathway in hepatocellular carcinoma. Mol Med Rep. 2013 May 31.
\n7. Holloszy JO. Regulation of Mitochondrial Biogenesis and GLUT4 Expression by Exercise. Compr Physiol. 2011 Apr;1(2):921-40.
\n8. O’Neill HM. AMPK and Exercise: Glucose Uptake and Insulin Sensitivity. Diabetes Metab J. 2013 Feb;37(1):1-21.
\n9. Sanchis-Gomar F. Sestrins: novel antioxidant and AMPK-modulating functions regulated by exercise? J Cell Physiol. 2013 Aug;228(8):1647-50.
\n10.Klarner A, von Stengel S, Kemmler W, Kladny B, Kalender W. Effects of two different types of whole body vibration on neuromuscularperformance and body composition in postmenopausal women.
\nDtsch Med Wochenschr. 2011 Oct;136(42):2133-9
\n11.Park SH, Huh TL, Kim SY, Oh MR, Tirupathi Pichiah PB, Chae SW, Cha YS. Antiobesity effect of Gynostemma pentaphyllum extract (actiponin): A randomized, double-blind, placebo-controlled trial. Obesity (Silver Spring). 2013 Jun 26. doi: 10.1002\/oby.20539.
\n12.Gauhar R, Hwang SL, Jeong SS, Kim JE, Song H, Park DC, Song KS, Kim TY, Oh WK, Huh TL. Heat-processed Gynostemma pentaphyllum extract improves obesity in ob\/ob mice by activating AMP-activated protein kinase. Biotechnol Lett. 2012 Sep;34(9):1607-16. doi: 10.1007\/s10529-012-0944-1
\n13.My own calculation, based on US incidence in 2004, medeconomic inflation and the relative size of the UK population.<\/p>\n","protected":false},"excerpt":{"rendered":"