10 ways to Prevent Obesity

Obesity:

Obesity often results in excessive calories’ intake than are burned by exercise and normal daily activities.
Obesity is a complex disorder involving an excessive amount of body fat. Obesity isn’t just a cosmetic concern.

The most common causes of obesity are overeating and physical inactivity. Ultimately, body weight is the result of genetics, metabolism, environment, behaviour, and culture.

Genetics.

A person is more likely to develop obesity if one or both parents are obese.

The excessive body fat increases the risk of serious health problems such as heart disease, diabetes and high blood pressure. The mainstay of treatment is lifestyle changes such as diet and exercise.

Types of body fat:

The visceral fat is the fat that is in the internal abdominal cavity, surrounding the vital organs in the trunk (abdominal) area.

The hypodermics are beneath dermis which is beneath the epidermis. It is used mainly for fat storage. A layer of tissue lies immediately below the dermis of vertebrate skin. It is often referred to as subcutaneous tissue.

Subcutaneous fat is normally harmless and may even protect against some diseases.

The body fat percentage of a human or other living being is the total mass of fat divided by total body mass, multiplied by 100; body fat includes essential body fat and storage body fat.

Essential body fat is necessary to maintain life and reproductive functions. Healthy body-fat percentage ranges based on your fitness level, follow these guidelines: Top athletes: 15 to 20% Fit women: 21 to 24% Healthy/acceptable: 25 to 32%

The factors weight gain, obesity and metabolic disease, many of which have nothing to do with willpower.

Body mass indexes are a parameter to gauge the body fat deposition in the body.

1. Genetics

Children of obese parents are much more likely to become obese than children of lean parents.

2. Engineered Junk Foods

These products are designed to be cheap, last long on the shelf and taste so incredibly good that they are hard to resist and they also promote overeating.

3. Food Addiction

Many sugar-sweetened, high-fat junk foods stimulate the reward centres in your brain. Junk foods can cause addiction in susceptible individuals. These people lose control over their eating behaviour.

Addiction is a complex issue that can be very difficult to overcome. When you become addicted to something, you lose your freedom of choice and the biochemistry in your brain starts calling the shots for you.

4. Aggressive Marketing

Junk food producers are very aggressive marketers. Their tactics can get unethical at times and they sometimes try to market very unhealthy products as healthy foods. These companies also make misleading claims.

What’s worse, they target their marketing specifically towards children.

In today’s world, children are becoming obese, diabetic and addicted to junk foods long before they’re old enough to make informed decisions about these things.

5. Insulin

Insulin is a very important hormone that regulates energy storage, among other things. One of its functions is to tell fat cells to store fat and to hold on to the fat they already carry.

The Western diet promotes insulin resistance in many overweight and obese individuals. This elevates insulin levels all over the body, causing energy to get stored in fat cells instead of being available for use.

While insulin’s role in obesity is controversial, several studies suggest that high insulin levels have a causal role in the development of obesity

6. Certain Medications

Many pharmaceutical drugs can cause weight gain as a side effect.

For example, antidepressants have been linked to modest weight gain over time.

Other examples include diabetes medication and antipsychotics.

These drugs don’t decrease your willpower. They alter the function of your body and brain, reducing the metabolic rate or increasing appetite

7. Leptin Resistance

Leptin is another hormone that plays an important role in obesity. It is produced by fat cells and its blood levels increase with higher fat mass. For this reason, leptin levels are especially high in people with obesity.

In healthy people, high leptin levels are linked to reduced appetite. When working properly, it should tell your brain how high your fat stores are.

This condition is called leptin resistance and is believed to be a leading factor in the pathogenesis of obesity.

8. Food Availability

Junk food is available everywhere now. Shops display tempting foods where they are most likely to gain your attention.

Another problem is that junk food is often cheaper than healthy, whole foods, especially in America.

Some people, especially in poorer neighbourhoods, don’t even have the option of purchasing real foods, like fresh fruit and vegetables.

Convenience stores in these areas only sell sodas, candy and processed packaged junk foods.

9.Sugar

Added sugar changes the hormones and biochemistry of your body when consumed in excess. This, in turn, contributes to weight gain.

Added sugar is half glucose, half fructose. People get glucose from a variety of foods, including starches, but the majority of fructose comes from added sugar. Excess fructose intake may cause insulin resistance and elevated insulin levels. It also doesn’t promote satiety in the same way glucose does

For all these reasons, sugar contributes to increased energy storage and, ultimately, obesity.

Weight Control and Obesity Prevention

The following are the essentials factors:

1-Dieting :

Very low caloric/energy density diets (<800 kcal/day) resulted in the greatest weight loss, ∼15–25% of initial weight, over a short period, in those who completed the programme.2,3 However, the authors noted that these programmes were associated with a high financial cost, high attrition rates and high odds of regaining 50% or more of the lost weight over 12–24 months of follow-up. A moderate weight loss (up to 3% of original weight) over 2 years of follow-up, trials of self-help programmes and programmes available over the internet do not suggest benefits in terms of weight loss or other outcomes.

In the long-term, only low-fat diets have been found to be beneficial, with a pooled weight loss of −3.55kg (95% CI −4.54 to −2.55kg) at 36 months compared with control groups. There were also long-term beneficial effects on dyslipidaemia and blood pressure for low-fat diets in obese individuals.

2-Pharmacological treatment

Two anti-obesity drugs—Orlistat and Sibutramine—have been widely assessed in a number of randomized controlled trials.

Orlistat, a pancreatic lipase inhibitor that reduces the absorption of dietary fat, is effective both in the short-term and long-term at reducing weight, particularly when combined with dietary and exercise interventions.

The combination of orlistat and physical activity advice has been found to have long-term (18–24 months) beneficial effects on dyslipidaemia and hypertension, Orlistat is associated with a higher incidence of gastrointestinal adverse events, which have in some trials resulted in poor compliance.

Further, there is some evidence that the effect of Orlistat, in terms of weight loss and improvements in cardiovascular disease risk factors, is weaker for obese individuals who are also diabetic than for non-diabetic obese individuals.

Sibutramine is a centrally acting serotonin–Norepinephrine reuptake inhibitor that enhances satiety and promotes energy expenditure. Short-term trials and one trial over 2 years of follow-up demonstrate sustained effects on weight loss.

Beneficial effects of Sibutramine on triglyceride, high-density lipoprotein cholesterol, and glycaemic control have also been reported, but there is no direct evidence that Sibutramine reduces obesity-associated morbidity and mortality.

As its Norepinephrine effect, it has been anticipated that Sibutramine could increase blood pressure. This hypothesis is supported by some, though not all trials.

Nevertheless, it is not recommended for use in obese individuals with hypertension, which, given the concordance between obesity and hypertension, somewhat limits its usefulness.

Many new pharmacological approaches are under investigation. These include gut hormones: such as cholecystokinin that normally signal satiety,

other centrally acting serotonin agents, the anticonvulsant medications topiramate and zonisamide, cannabinoid receptor antagonists, and drugs that act on other peptide neurotransmitters.

The first randomized controlled trial (n = 1507) in humans of a selective cannabinoid-1 receptor antagonist (rimonabant) was recently published.10 It found a marked reduction in weight and waist circumference and improvements in high-density lipoprotein cholesterol, triglycerides, insulin resistance, and the prevalence of the metabolic syndrome at 1 year of follow-up when rimonabant was given at a dose of 20 mg per day, but much weaker effects on weight reduction of a 5 mg dose and no effects on metabolic syndrome components at this lower dose.

Despite the marked weight loss with the higher dose, there was no effect on blood pressure, total cholesterol, or low-density lipoprotein cholesterol. Further, there is evidence from animal studies that low dose cannabinoid therapy reduces the progression of atherosclerosis, and it has, therefore, been suggested that blocking cannabinoid receptors might actually increase the risk of atherosclerosis.

There is biological evidence that blocking cannabinoid receptors might result in demyelination and one participant treated with rimonabant in this trial developed multiple sclerosis.

Diet programs may produce weight loss over the short term, but maintaining this weight loss is frequently difficult and often requires making exercise and a lower calorie diet a permanent part of an individual’s lifestyle. Success rates of long-term weight loss maintenance with lifestyle changes are low, ranging from 2 to 20%. Dietary and lifestyle changes are effective in limiting excessive weight gain in pregnancy and improve outcomes for both the mother and the child. The National Institutes of Health recommend a weight loss goal of 5% to 10% of the person’s current weight over six months

3.Surgery.

Ideally, any treatment for obesity should assess long-term impacts on obesity-associated cardiovascular risk factors, such as hypertension, dyslipidaemia, and insulin resistance, as well as disease outcomes such as cardiovascular disease, diabetes, and osteoporosis. However, to date, few studies of any intervention have been sufficiently powered and sufficiently long-term to go beyond the assessment of weight loss itself.

4-Physical exercise

The evidence suggests that regular exercise can be an important factor in the development of sustained negative energy balance conditions provided the volume of activity is high. This implies a program of low to moderate-intensity exercise performed on an almost daily basis for at least one hour per session. To induce significant weight and fat losses and to treat overweight and obese patients, compliance with the program for several years becomes a necessity. Exercise increases lipid substrate oxidation and may favour carbohydrate intake for the same amount of energy intake. The acute effects of exercise on resting metabolic rate are well documented, but the long-term influences of exercise training seem to be small and are rapidly suppressed with the cessation of training. The obese benefits also from a regular exercise regimen in terms of improved insulin sensitivity, lipid and lipoprotein profile, and blood pressure, as well as reduced risk of death. Regular exercise, such as walking, is a healthy course of action for overweight or obese patients

The most effective treatment for obesity is bariatric surgery. Surgery for severe obesity is associated with long-term weight loss and decreased overall mortality. One study found a weight loss of between 14% and 25% (depending on the type of procedure performed) at 10 years, and a 29% reduction in all-cause mortality when compared to standard weight loss measures.

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