From healthy eating to drug: Beat obesity most effectively

Obesity has become a significant global health challenge with an increasing prevalence in both developed and developing countries. The worldwide occurrence of obesity has nearly tripled in the last 40 years, and 31.3 per cent of India’s population was diagnosed positive in the year 2015. 

 Obesity is associated with a plethora of metabolic diseases including cardiovascular anomalies, hypertension, diabetes mellitus, dyslipidemia, and sleep apnea. The primary cause of obesity may be genetic—including monogenic disorders and conditions like Prader—Willi. Secondary causes may be neurological illnesses like brain injury, tumours, hypothalamic obesity), endocrine imbalances like hypothyroidism or depression or drug-induced problems like the effects of antidepressants and beta-blockers. 

Obesity causes decreased cardiac output, increased left ventricular wall thickness and accelerates atherosclerosis. It also results in diabetes by altering levels of adipocytokines, increasing circulation of free fatty acids and altering body fat distribution, causing insulin resistance and increased blood glucose levels. Weight loss can bring in significant differences in this condition. A loss of 5-10 per cent has been shown to improve hypertension, insulin resistance, and glycemic control. In the diabetes prevention program, a cut-back of approximately 7 per cent achieved through lifestyle changes was associated with a 58 per cent reduction in the risk of developing type 2 DM in obese, prediabetic individuals. A weight loss of 10 kg increased life expectancy by 35%.  

While many methods for weight loss are available these days, lifestyle interventions and maintaining a healthy diet are most preferred. All scientific guidelines mandate at least 150 minutes of moderate aerobic exercise per week, along with 3 weekly sessions of resistance training. Mediterranean diet which is rich in vegetables, fruits, lean meat and fish cooked in olive oil is shown to aid in weight loss. 

Drug therapy is indicated when lifestyle interventions fail in long-term weight management of patients who are obese—with body mass index >30 kg/m2 or those who have BMI between 27-29.9 with obesity-related morbidity (eg diabetes, hypertension, etc). Doctors were facing a holy grail when it came to safe and effective anti-obesity molecules for non-diabetic obese patients until we found the answer in lorcaserin.

This drug is promising as it acts on the 5HTc receptor selectively and stimulates them in the appetite center of the brain. This further reduces food intake and increases a feeling of fullness, thus aiding weight loss. Compared to other similar molecules it has fewer cardiovascular side effects like valvular heart disease. 

It helps in effective weight loss when taken on a long term basis accompanied by exercise and diet control. This, in turn, will reverse many of the obesity-related complications mentioned earlier too. However, It cannot be used in those with major depressive disorders. Surgery is yet another way to beat extreme cases of obesity. Bariatric surgery is a good option for those with a BMI above 40, but all surgeries have their own set of complications. An appropriate weight-loss strategy must be chosen only after taking aspects like cardiovascular safety, and maintenance of kidney health into account.

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What is Prader-Willi syndrome?

Prader-Willi syndrome (PWS), an unusual genetic disorder that leaves one constantly hungry.

Prader-Willi syndrome is a debilitating condition that occurs in roughly 1 out of every 15,000 births. A nonprofit dedicated to PWS defines it as “a complex genetic disorder affecting appetite, growth, metabolism, cognitive function, and behavior.” The condition is marked by a dysfunction of the hypothalamus, which regulates hunger.

Scientists have narrowed down the cause of the condition to an abnormality of chromosome 15 but have yet to determine what sparks the abnormality in the first place.

The first signs of PWS begin in infancy, with weak muscles, difficulty feeding, and delayed development. By early childhood, the condition begins to manifest as an insatiable appetite, which often leads to overeating and, in turn, early-onset obesity. As people with PWS get older, they often experience intellectual disabilities (either mild or moderate) and exhibit specific characteristics such as small hands and feet, a narrow forehead, and short stature.

Due to their insatiable appetite, people with PWS are more likely to develop type II diabetes and to experience other obesity-related health conditions. According to the Foundation for Prader-Willi Research, the condition can be diagnosed through a blood test at birth, and early treatments such as human growth hormone (which people with PWS are deficient in) can help.

But as with many rare genetic disorders, scientists are still working to fully understand PWS. As it stands now, controlling the desire to overeat remains the biggest obstacle to a normal life.

THIS IS ONLY FOR INFORMATION, ALWAYS CONSULT YOU PHYSICIAN BEFORE HAVING ANY PARTICULAR FOOD/ MEDICATION/EXERCISE/OTHER REMEDIES.                                                                                                                                                                                                      PS- THOSE INTERESTED IN RECIPES ARE FREE TO VIEW MY BLOG-                                                                                           https://gseasyrecipes.blogspot.com/   

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Gene mutations linked to severe obesity

Increasingly research is revealing that not only lifestyle factors, but genetics also play an important role in determining an individual`s susceptibility to obesity.

Identifying the mutations that underlie the fraction of obese patients with monogenic obesity can help us to understand complex processes like metabolic rate, eating behaviour, growth, and fat storage.

In a new study, two groups have identified obesity-linked mutations in the gene SIM1.

Sadaf Farooqi and colleagues at Addenbrooke`s Hospital in Cambridge, England, identified thirteen SIM1 mutations in obese patients, and found that reduced SIM1 function correlated with increased food intake and altered nervous system dysfunction.

In an independent study, Philippe Froguel and colleagues at Imperial College London identified eight SIM1 mutations in morbidly obese adults and in patients with a disorder resembling Prader-Willi syndrome.

In the patients studied, loss of SIM1 function was associated with inherited obesity. Taken together, these studies confirm a strong link between SIM1 dysfunction and obesity.




ps- this is only for information, always consult you physician before having any particular food/ medication/exercise/other remedies.

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