Biomechanics of the Knee & Weight Gain
Osteoarthritis (OA) and obesity evolve over a lifespan and are both chronic conditions. The Harvard Clinical and Translational Science Center describes osteoarthritis (OA) as a progressive degenerative joint disorder. In a normal joint the articular cartilage is a protective surface membrane found diffusely at the joint surfaces, which provides support and lubrication for healthy knee function.
In OA the kinematic and biomechanical changes affect the articular cartilage, causing subchondral bone remodeling (bone cysts, bone collapse, etc), degeneration of menisci and ligaments, joint capsular hypertrophy, and the synovial and osteophytic enlargements. All of which are associated with OA pathogenesis (Harvard, 2017).
When the joint articular cartilage covering the bones of the knee wears away, it leaves bare bones in contact with each other causing mild to severe unremitting pain and swelling.
Additionally, obesity has been linked to early structural changes including the presence of cartilage defects (Wang, 2007). “With increasing obesity, joint loading, as well as fat mass, become greater. Higher levels of adiposity are accompanied by metainflammation, with production of adipokines and proinflammatory cytokines. The combined effect of adipocytokines and increased loading can facilitate the pathogenesis of OA, affecting bone, cartilage and synovial tissue.” (Wluka, 2012)
It is therefore important to note that the rate of change in obesity over time does affect risk and development of knee OA. In obese patients the chronic load results in increased risk of incident OA, since it directly impacts the joint tissue structure and biomechanics (Sowers, 2010). Nonetheless, variety of genetic and environmental factors contribute to OA onset and progression, leading to the same pathological end point. The normalized body weight, muscle mass, muscle strength collectively decrease OA progression. In contrary to muscle mass, fat mass increase the chance of joint-space width (Sowers, 2008), cartilage defects (Berry, 2010), and cartilage loss (Cicuttini, 2005).
“Obesity can affect the pathogenesis of OA through biomechanical effects as well as via increased metainflammation. Increased obesity is associated with higher levels of joint loading and reduced levels of physical activity, which in turn reduces muscle strength. Combined, these effects can result in the structural changes of OA. Structural disease results in pain, which presents a barrier to physical activity, further reducing energy expenditure and resulting in reduced muscle mass and increased fat mass. Thus, these factors may contribute to a vicious cycle of obesity and OA. Abbreviation: OA, osteoarthritis.”
The relationship between obesity and OA is not simple, encompassing a variety of influences that include mechanical loading, muscle function, and metabolic and behavioural factors .
“The approach taken will depend on whether society deems that this issue is of collective or individual responsibility. Individualist approaches have been trialled with limited success — a societal strategy is needed, but it remains far from clear which will be appropriate. As symptomatic and structural disease severity progresses and has an increasing impact on function and quality of life, management aims should increasingly emphasise weight loss. Weight loss and maintenance strategies that incorporate muscle strengthening exercises might improve symptomatic outcomes. However, even in the absence of exercise, weight loss is achievable; thus, difficulty in undertaking exercise should not be raised as a barrier to attempt weight loss. Although future work is needed to understand the role of metabolic factors in disease pathogenesis, and the relationship between weight loss and risk of OA incidence and progression, these details will inform only a reactive approach to the problem. A more proactive and effective strategy might well require societal and cultural changes with regards to diet, physical activity, food marketing and agricultural subsidies. To date, strategies at the individual level have been costly, both in human and financial terms: a more effective, coordinated societal approach is required” (Wluka, 2013).
Ketogenic diet & Sportsmanship
The father of modern medicine Hippocrates advised “Let your food be your medicine, and your medicine be your food” (Singh, 2014. p.3). The ketogenic diet is characterized as low carbohydrate, high fat, and moderate protein, or low carbohydrate, low fat and moderate protein content. Although carbs are excluded from the diet as a source of fuel to the brain and skeletal muscles, ketone bodies with βhydroxybutyrate and acetoacetate contained in high fat diet are the alternative energy resources. During endurance training such as triathlon, marathon, and cross country cycling fat oxidation is the most significant metabolic adaptation, since it provides with cognitive and muscular strength for athletes. During aerobic system training for example, the total allowance of fatbased energy source exponentially increases. Now the muscle of athletes uses larger mitochondrial density, that helps them to oxidize more fat as fuelsource, which enables with longer exercise time prior and postponed experiences of glycogen exhaustion and fatigue. Furthermore, athletes during exercise deliver more oxygen and blood flow to the muscles as a result of arteriovenous oxygen variance and increased cardiac functions (Zajac, 2014, p.2495). These processes promote fat oxidation at higher rate, ergo differentiate “ketonefueled” athletes from carbohydrateusers. As a result, athletes who obtain energy from ketones perform with more efficiency for longer timeperiod, while athletes whose carbohydrate loading metabolized at higher speed, are left with no energy fuel to continue their exercise within a much shorter timespan.
Fasting and Weight Loss
An alternative approach to the weight loss paradigm as recommended by Stephanie Bair from Stanford university is the intermittent energy restriction (IER) alternative (Harvie, 2010). IER refers to restrictive daily calorie intake, which could be performed in a number of ways.
- A 24 to 36 hours fasting period once a week;
- confining meal intake to a 6–8 hour daily timeframe;
- or severely restricting calorie intake to 400–500 total calories per day.
If there are no medical condition cautioned by your physician to avoid fasting, you may start at any time. There are many forms of fasting and dieting, and due to our individual differences it may take some experimentation to explore what fits YOUR body best. For example, first of 500–600 calorie diet is no picnic. Be smart and pick your favourite food day by day, one at the time. Gradually, the initial feeling of deprivation will fade and lessen.
Dr. Michael Mosley and Mimi Spencer in his recent book the FastDiet strategized on managing appetite temptations and strengthening one’s willpower in making prudent and healthy snacking choices. Dr. Mosley described that on average we make 227 food-related choices daily (Wansink, 2007), and in order to control our habits we must identify in advance our temptations. Specifically, he advised:
- Know your triggers: as a rational being you are in power to select or ignore each food craving experience. This takes grit and willpower. The appreciation of this power will promote deliberate practice, which ultimately allows overcoming the cognitive bias of cravings. For instance, instead of midnight snacking choose to drink a cup of green tea. instead of late-night fridge raid take a shower/bath. If you are prone to ordering desert at restaurants choose to have your lunch at the office or near-by public park.
- Know temptations are fast-coming and fleeting: distract your mind for 2–5 minutes. Meditate with deep breath, drink a cup of water or green tea, call a friend for a minute, walk and talk to your co-worker.
- Exercise the “Proximity Principle” and store temptations distantly: the International Journal of Obesity published a case study showing that candies stored conveniently close to hand were consumed at a significantly higher rate compared to those not as visible and easily accessible. A good strategy is to replace unhealthy cookies with fresh/dried/frozen fruits to consume as snacks (Wansink, 2006).
- Remember that your goal overweights your temptation: it is important to recall what made you decided to start loosing weight: longer life, healthy body, better cognitive performance, smaller medical bills. Take a photo of yourself and tape it on your fridge door to serve as reminder.
- Exercise willpower: Kelly McGonical from Stanford University wrote an entire book The Willpower Instinct: How Self-Control Works, Why It Matters, and What You Can Do to Get More of It, suggesting that willpower should not be perceived as integrity but instead as a muscle; the more the “willpower” muscle is exercised the stronger it becomes.Thus perseverance in willing to overcome temptations will promote ease in losing weight.
In all, healthy dieting will promote your longevity and prolong healthy long life.
Dr. Michael suggest that once the target weight is reached the Maintenance model should be introduced to support the healthy BMI. Weight loss will promote BMI and body fat measurements to drop; the cholesterol count, IGF-1, and blood glucose level to improve. Factors that will promote longevity and health.
There is overwhelming scientific evidence that a low carb Mediterranean-style diet — one rich in vegetables, olive oil, nuts and the occasional glass of wine or bite of dark chocolate — is better for weight loss, blood sugar control and improving cholesterol than going on a low fat diet. That’s why it’s central to the Blood Sugar Diet.
- Learn more about the Fast diet and to join the society: https://thefastdiet.co.uk/forums/
- Learn more about the https://thebloodsugardiet.com
- Take a self- assessment quiz to find out if you are addicted to carbs: https://thebloodsugardiet.com/quizzes/are-you-addicted-to-carbs/
- Join a 12-Weeks Online Blood Sugar Diet Program: https://thebloodsugardiet.com/12-week-online-program/ . This program was carefully planned by doctors, dietitians and exercise coaches.
Bali, A. (2015). Psychological Factors Affecting Sports Performance. International Journal of Physical Education, Sports and Health, 1: 9295, http://www.kheljournal.com/archives/2015/vol1issue6/PartB/1577.pdf
Benton, D., Donohow, R.T. (1999). The effects of nutrients on mood. Public Health Nutrition. 2(3A): 403409 https://vpn2.ucsd.edu/+CSCO+0h756767633A2F2F77626865616E79662E706E7A6F65767174722E626574++/action/displayAbstract?fromPage=online&aid=554828&fileId=S13689 80099000555
Halyburton, A. K., Brinkworth, G. D., Wilson, C. J., Noakes, M., Buckley, J. D., Keogh, J. B., and Clifton, P. M. (2007) Low and highcarbohydrate weightloss diets have similar effects on mood but not cognitive performance. The American Journal of Clinical Nutrition. 56:580587 http://ajcn.nutrition.org/content/86/3/580.full.pdf+html
Harvey, M.N., Pegington M, Mattson MP, Frystyk J, Dillon B, Evans G, Cuzick J, Jebb SA, Martin B, Cutler RG, Son TG, Maudsley S, Carlson OD, Egan JM, Flyvbjerg A, Howell A. The effects of intermittent or continuous energy restriction on weight loss and metabolic disease risk markers: a randomized trial in young overweight women. International Journal of Obesity. 2011. 35(5):714–27. https://www.ncbi.nlm.nih.gov/pubmed/20921964
Murphy, P., Likhodii, S., Nylen, K., Burnham, W.M. (2004). The Antidepressant Properties of the Ketogenic Diet, Biological Psychiatry, 56: 981983. http://www.biologicalpsychiatryjournal.com/article/S00063223(04)010066/abstract
Orlick, T., Partington, J. (1988). Mental Links to Excellence. The Sport Psychologist, 2: 105130, http://web.natur.cuni.cz/~houdek3/papers/Orlick%201988.pdf
Paoli, A., Bosco, G., Camporesi, E.M., Mangar, D. (2015) Ketosis, ketogenic diet and food intake control: a complex relationship. Frontiers in Psychology. http://journal.frontiersin.org/article/10.3389/fpsyg.2015.00027/full
Singh, M. (2014). Mood, food, and obesity. Frontiers in Psychology: Eating Behavior. 5(925): 111, http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4150387/pdf/fpsyg0500925.pdf
Volek, J. S., Noakes, T., & Phinney S. D. (2015). Rethinking fat as a fuel for endurance exercise, European Journal of Sport Science, 15:1320. http://www.ncbi.nlm.nih.gov/pubmed/25275931
Wansink, B., Painter, J.E., Lee, Y.K. The Office Candi Dish: Proximity’s Influence on Established and Actual Consumption, International Journal of Obesity, 2006. Print.
Wansink, B., Sobal, J. Mindless Eating: The 200 Daily Food decisions we Overlook, Environment and Behavior. 2007. Print.
Zajac, A., Poprzecki, S., Maszczyk, A., Czuba, M., Michalczyk, M., and Zydek, G. (2014) . The Effects of a Ketogenic Diet on Exercise Metabolism and Physical Performance in OffRoad Cyclists. Nutrients. 6: 24932508. http://www.ncbi.nlm.nih.gov/pubmed/24979615
Wang, Y. et al. Body composition and knee cartilage properties in healthy, community-based adults. Ann. Rheum. Dis. 66, 1244–1248 (2007).
Ding, C. et al. Association between leptin, body composition, sex and knee cartilage morphology in older adults: the Tasmanian older adult cohort (TASOAC) study. Ann. Rheum. Dis. 67, 1256–1261 (2008).
Sowers, M. R. & Karvonen-Gutierrez, C. A. The evolving role of obesity in knee osteoarthritis. Curr. Opin. Rheumatol. 22, 533–537 (2010).
Sowers, M. F. et al. BMI vs body composition and radiographically defined osteoarthritis of the knee in women: a 4-year follow-up study. Osteoarthritis Cartilage 16, 367–372 (2008).
Berry, P. A. et al. The relationship between body composition and structural changes at the knee. Rheumatology (Oxford) 49, 2362–2369 (2010).
Cicuttini, F. et al. Association of cartilage defects with loss of knee cartilage in healthy, middle-age adults: a prospective study. Arthritis Rheum. 52, 2033–2039 (2005).