Osteoporosis - an Evolutionary Perspective - Literature review Example

Osteoporosis: An Evolutionary Perspective Names: Date: Institution: Introduction The universal trend towards an increase in longevity has without a doubt been a marked feature of the 21st century and which has consequently translated to aging populations as well as the increase in diseases and conditions affecting older people. One of these conditions is the globally recognized osteoporosis. Osteoporosis, defined as the skeletal disorder that is basically characterized by the compromised bone-strength predisposing individuals to higher fracture risks, indeed has serious determinants and consequences, at least from an evolutionary perspective. With regards to this, this particular paper gives a detailed account of osteoporosis through an evolutionary perspective. For over one century after the hunter died, osteoporosis was still not a recognized condition. A positive step towards this direction was actually made around 1930s by a French pathologist known as Jean Georges Frederic Martin Lobstein. He recognized that many people in their 30s and 40s tended to develop bent backs. Later on this disease was recognized as associated with multiple vertebrae problems with high frequencies reported among older people. According to Genet (2008), the number of the elderly and those aging has increased due to an increase in life expectancy. In a similar manner, an increase in the number of people living with osteoporosis has also been recorded. Osteoporosis, which is basically a systematic condition coming with age, has been noted as occurring more naturally while affecting humans only. In fact, cotter et al (2011) highlight that humans have high susceptibility to osteoporosis as well as its related fractures due to the evolutionary adaptations witnessed. According to Karasis (2008), the human evolution principle seems to highlight osteoporosis as highly heritable therefore easily transmitted from one generation to the next. According to Alder (2010) osteoporosis has a strong genetic component highly comprising reduced bone mass and a high risk of fragility. Bone mineral density (BMD) has widely been used to diagnose osteoporosis. Following a decade of hunting for genes, there has been findings that, despite the main roles of the environment in this, genes of osteoporosis actually exist and have been transferred from ancestors/grandparents to individuals. In fact, assemblies of many genes with several individual effects determine the component of osteoporosis. In this case, each gene is responsible for less than 5% of the variance of genetics in the entire population. On the other hand, there are various studies and methods that have been fundamental in identifying the susceptibility of osteoporosis. The first one regards the candidate-gene association. Following a discussion on vitamin D receptor (VDR) that was published ten years ago, there has been a significant increase in the number of research studies concerning genetic associations. The difference most notable as compared to that of the past is the use of bigger samples and a consideration of multiple variants and heliotypes with the inclusion of gene-gene and interactions of gene-environment. Actually, the Genetic Markers of Osteoporosis (GENOMOS) comprised many gene polymorphism related to osteoporosis. The role of gene encoding was evaluated on alpha 1 chain of type I (COLIA1) Sp 1 alleles a BMD and fracture predictor. It involved an approximated 20,786 people and whose later results brought to the fact that COLIAL Sp 1 polymosism is connected to minimizing BMD and can lead to vertebral fractures in women free from BMD. 63 genes were related to BMD phenotypes related to osteoporosis by the end of 2005. More than 4 independent sampled replicated 16 genes, 18 genes in 1-3 sovereign samples and 29 genes had BMD in a particular sample (Duque & Kiel, 2008). However, there have been cases of unreliability and inconsistency from previous results. Thus, the method that has been used to successfully describe the role of many candidate genes in osteoporosis is Meta analysis which has identified discrepancies successfully. Another study done on genes was family based linkage study on cloning position of BMP2. A bone morphogenetic protein 2 gene (BMP2) was the first osteoporosis gene in humans that was identified by positional cloning and linkages. A detection of a linkage signal on 20p12 to the risk of osteoporosis was made in an Iceland population. It was found that BMP2 is associated the risk of osteoporosis and BMD accounting to part of the identified linkage signals. On natural selection in osteoporosis, Smith & Frame (1964) argued that there is no selection against osteoporosis phenotypes because they later cause problems in life with no early effect in life. A child with pro-osteoporotic architecture of the bone, with lower bone mineralization would in future transfer these genes. Impaired intestinal calcium absorption from negative D deficiency has been identified as a possible factor in women’s negative calcium balance with skeletal atrophy. The measurement of blood index done was called SARA (Serum antirachitic activity). A study on Puerto Rican women actually found that the women had higher levels. There was observation of high levels of phosphorus and serum calcium. This is because serum samples from women with disorder had antirachitic levels lower than from those women without. Environmental changes among hominids are other factors that have been argued to cause osteoporosis. Anthropometric factors and lifestyle issues form part of the environmental factors. In fact diet, just as lifestyle, is a significant factor here. The two are considered as greatly influencing susceptibility to various diseases. Osteoporosis is actually regarded as a lifestyle disease, longevity disease and the civilization disease. With reference to the latter, osteoporosis has been noted to seemingly increase in its frequency as various countries increasingly become industrialized and individuals increasingly live longer. The diets and sedentary lifestyle as a result of industrialization have changed significantly and are seen in numerous cases. Taking alcohol, low calcium intake, low body weight, reduced physical activity, increased intake of sugar and Smoking all highlight this. With reference to smoking, a study was done on female nurses totaling about 116,229 and who were between the ages 34-59. In a 12 year trends the results showed an increase in fracture towards female smokers. Compared to non smokers, the risk was 1.3. Ten years later after cessation, there were indications of people stopping smoking. In men, smoking raised bone resorption without any increase in the bone formation. Past smokers had a lower BMD compared to non smokers but with lack of improved resorption. This is because smoke from the cigarette extracts reduces in vitro differentiation of human osteoprogenitor cells to cells like osteoblast. In terms of increased sugar intake, the intake of high levels of sugar has been indicated as directly related to higher diabetic cases. Diabetes, which is also a noteworthy disease of civilization, is further noted to have very positive connotations with osteoporosis making it a great determinant of osteoporosis. Diabetes 2 lowers the density of the bone through an unknown mechanism. The bone density then declines due to a speed up by the hyperthyroidism. The absorption of phosphate and calcium is then interfered with by digestive disorders. Due to a decline in the mass of the bone it can easily cause fracture and lead to osteoporosis. In an analysis done among 398 outpatients, there were results on risk factors related to osteoporosis and diabetes complications. The comparison was between patients with diabetes type 2 and controls based on the population. The adjusted BMD found in both genders between type 1 and 2 was not different. However, compared to controls, it was higher in type 2 diabetes. The levels of osteoporosis at femoral neck –BMD was higher than that of lumbar spine- BMD. There was a positive correlation between BMD with BMI and a negative correlation with age. The fracture of fragility was low and indifferent to diabetes groups. The patients with fracture had low BMD levels compared with those that had no fracture. The specific parameters of diabetes do not in any way predict BMD. There is a low level of BMD both in diabetes type one and type two. The occurrence of fracture in both levels however is similar. It is however unrelated to the Tscore threshold which is less than -2.5, an underestimated problem that is common among diabetes patients (Oschman, 2011). Osteoporosis is also argued to have haunted more women since the dawn of the human history. Gender is thus highlighted as among the major factors that influence osteoporosis. The bone strength between men and women has been noted to differ. A particular study on heritability of BMD among 3,320 southern Chinese people was conducted in approximately 1,019 families. Using the variance component model, the results actually indicated a genetic difference in the hip and not the spine. The females had 0.63-0.71 BMD heritability in age, height and weight. That of men was 0.74-0.79 (Karasik, 2010). In a further research done on 297 female alcohol drinkers and 48 non alcoholic drinkers, moderate consumption of alcohol was associated with lumbar spines and distal radius of higher BMD. Drinkers had low markers of turnover and low parathyroid levels an indication that alcohol reduced the remodeling of the bone. Similarly, inadequate calcium diet with low levels of vitamin D causes the impairment of calcium absorption therefore increasing the levels of parathyroid hormone. This leads to an increase in bone resorption and hastened bone loss. Serum is needed for maximal absorption of calcium and optimal health. Vitamin D and supplements of calcium relatively increase BMD which eventually reduces the risk of fracture. A study on the lifestyle’s effects on low BMD was done in 418 southern Chinese women between the ages of 20-39. This was to identify clinical bone mass predictors in young premenopausal women. Low body weight was associated with 8-3 fold and a 6-8 risk in fold for having low BMD in the spine and hip. Heights below 153 cm were associated with risks in small bone areas. Physical inactivity on the other hand was associated with 2.8 folds of low spine and hip risks. Furthermore, Patlak (2001) indicates that women having postmenopausal osteoporosis often experience several fractures in bones located in the spine (vertebrae) while aging. As a consequence, the vertebrae often tend to collapse thereby forcing their spines to curve. The curvature thus results in height loss, a ribcage that is tilted, an abdomen that protrudes and the dowager’s hump. Nutritional history plays a role in the development of osteoporosis and the intake of food differing among examined species. Alder (2010) argues that it is unlikely that wild apes get better nutrition compared to the modern human being. There have been aspects implicated on agricultural based diet to help the reduced bone mass in the current human being. While there is a likelihood of nutrition contributing to differences among species, one cannot explain the increase in height, volume, and cross sectional areas of human vertebrate bodies in contrast to apes. Paleolithic humans were used to eating food that was generally available to them in their local environment. Their nutritional needs were shaped therefore by these foods unlike the current Neolithic times With time there emerged a change in the human diet due to agricultural and industrial revolution. The agricultural developments and industrial revolution then brought changes to the diet of humans. Over 5000 to 10000 years ago, revolution in agriculture replaced the uncultivated food with grains and dairy. In fact, in most of the western nations, people began eating more vegetable oils, meat, alcoholic beverages/drinks, dairy products and sugary foods in the last half of the 20th century Key et al (2002). As well, people began living sedentary lifestyles which in addition to their changed diet developed a myriad of diseases including the current osteoporosis. Currently, it can be argued that the human genome has been chosen by natural selection for ancestral Paleolithic environment, the natural selection where the western culture quickly influences the culture and lifestyle of Paleolithic humans. These changes had profound impacts but and caused health problems in the subsequent years. There have been arguments by Katz & Friedman (2008) on the matter above indicating that human beings can live healthily with a variety of diets. Similarly, there has been an evolution where human beings have tended to be flexible eaters. However, with different health consequences emanating from eating flexibly, research has been upfront in determining what really harms the introduced dairies and grains. The reality is, as much as the current human being is expected to eat like the Paleolithic, it can never be so in the current society. This is because every plant and animal consumed by human beings has evolved to fit the dietary needs of the modern society. While the introduction of grains, legumes and dairy products has evolved over the years hence becoming prone to various diseases, it is enough to conclude that if human beings could survive in the same environments as that of their ancestors then diseases like osteoporosis would not be existing today. Conclusion Osteoporosis is undoubtedly one of the many conditions that affect the older people. While it is clear that longevity is a fact of the 21st century and the increasing cases of osteoporosis can not be ignored anymore, various studies have deeply analyzed the reasons for the occurrence of osteoporosis and developed converging views. According to the above analysis, it is clear that the evolutionary perspective of osteoporosis contributes much towards the understanding of what underpins its occurrence. While the analysis has highlighted this condition based on evolution and its profound changes, it has similarly indicated various factors that are a determinant and that contribute significantly to the reported cases, including genetic factors, sedentary lifestyle, nutrition and gender. References Adler, R. A. (2010). Osteoporosis: Pathophysiology and clinical management. New York, NY: Humana Press. Cotter, et al. (2011). “Human Evolution and Osteoporosis-Related Spinal Fractures”. PLoS ONE 6(10): e26658. Duque, G. & Kiel, D. (2008). Osteoporosis in older persons: Pathophysiology and therapeutic approach. London: Springer. Genet, H. (2008). “Osteoporosis: an evolutionary perspective” Epub 124(4):349-56. Karasik, D., Hsu, Y.-H., Zhou, Y., Cupples, L. A., Kiel, D. P., & Demissie, S. (2010). Genome-wide pleiotropy of osteoporosis-related phenotypes: The framingham study. Journal of Bone and Mineral Research, 25, 7, 1555-1563. Karasik, D. (2008). “Osteoporosis: an evolutionary perspective.” Human Genetics, 124, 4, 349- 356. Katz, D. L., & Friedman, R. S. C. (2008). Nutrition in clinical practice: A comprehensive, evidence-based manual for the practitioner. Philadelphia: Lippincott Williams & Wilkins. Key, T. et al. (2002). “The effect of diet on risk of cancer”. Lancet, 14; 360(9336):861-8 Oschman, J. L. (2011). Chronic disease: are we missing something?.Journal of Alternative and Complementary Medicine. 17, 4, 283-5. 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