Medical Weight Loss Certification Training for Physicians, Nurse Practitioners, and Physician Assistants

medical weight loss certification

Medical Weight Loss Training provides you with our FREE Medical Weight Loss Certification Training Manual. Please contact us for your complete online training for physicians, nurse practitioners and physician assistants

How to start a medically supervised weight loss clinic: a Beginner’s Guide to Prescription Medications.

Introduction to Obesity

Obesity is defined as body mass index (BMI), which is a ratio of weight and height, greater than 30 kg/m2. BMI between 25 and 30 kg/m2 is considered overweight. An obese individual has amassed fat to the degree that it has multiple negative health effects, as it increases the likelihood of hypertension, diabetes, heart disease, specific cancers, and various other diseases.


Leptin, ghrelin, and other mediators are involved in the regulation of appetite, adipose tissue storage, and insulin resistance. Leptin signals the level of fat storage in the body. Produced by adipose tissue, leptin increases appetite when storage levels are low and decreases appetite when storage levels are high. Most obese individuals are categorized as leptin resistant and administration of leptin does not correct obesity in most patients. Ghrelin triggers an increase in appetite when the stomach is empty and is produced by the stomach. Both control appetite on the hypothalamus. Any deficiency or resistance along this pathway may contribute to obesity.

Anecdotal belief suggested that obesity was due to low metabolism, as obese people ate little, but gained weight. Research seems to indicate otherwise, as an obese individual typically has greater energy usage to maintain their increased BMI.

The major cause of obesity is excess consumption of food and inadequate physical activity. It is a simple math equation of input minus output. Additional causes of obesity can be attributed to genetics, medical or psychiatric illness. Many other societal influences contribute to the cause ranging from access to fast food, insufficient sleep, higher age of maternal pregnancy, and amount of automobile usage.


Since 1971, the average caloric increase is 335 calories per day in women and 168 calories per day in men. The primary source of the extra calories is due to sweetened beverages and potato chips. In addition, consumption of fast food meals quadrupled from 1971-2000. Within the same time frame, the obesity rate in the USA increased from 14% to 30%. Clinical tests also prove that obese patients consistently under-report their food consumption when compared to normal BMI patients. The national calorie consumption averages are 2800 calories per day for males and 1800 calories per day for females. The average person reports 30% – 40% less consumption than what one actually consumes in a day.

The average dinner plate has gotten larger in the past 50 years. Eating out has increased 200% from 1975 to 1997. A larger portion is also served in restaurants. While intake of fruits and vegetable serving is higher, up to 17% of all vegetable intake is due to potatoes in French fries. Cheese consumption is up, but due to pizzas and cheeseburgers.


Automotive transportation, labor-saving technology, and television have resulted in an increase in sedentary lifestyles. Up to 60% of the world’s population gets insufficient exercise.

Lack of sleep is associated with weight gain as less than 7 hours of sleep resulted in an increased risk of obesity. Less than 6 hours of sleep increased the risk to 27%. Children age 6 -12 who got less than 10 hours of sleep a night showed 3.5 times greater incidence of obesity than those who got 12 hours of sleep. It is believed that sleep deprivation leads to increased insulin, cortisol, and ghrelin, and decreased growth hormone and leptin. The current recommendation is that adults receive at least 7 hours of sleep, 8 hours optimally.


There is no evidence of a Mendelian pattern of inheritance. Adoptions studies show that there is a stronger correlation with biological siblings than with half-siblings. Also, adopted children had BMI that correlated with the biological parents than with adopted parents. Genes may play a role as research has shown that when food is abundant, genes controlling metabolism and appetite predispose a patient to become obese. Several rare genetic syndromes also cause obesity (Prader-Willi, Cohen, etc.).

Medical and psychiatric illnesses

Along with genetic causes, various congenital and acquired conditions such as Cushing’s syndrome, hypothyroidism, and other psychiatric disorders can contribute to obesity. Medications, such as insulin, antipsychotics, antidepressants, steroid, hormones, can also cause weight gains.

Health Effects

As one of the leading cause of preventable deaths, average life expectancy is reduced by six to seven years for obese patients. Severe obesity (BMI > 40) can reduce life expectancy by up to 10 years.

CDC states that overweight and obesity increase the risk of the following diseases.
Coronary heart disease
Type 2 diabetes
Cancers (endometrial, breast, and colon)
Hypertension (high blood pressure)
Dyslipidemia (for example, high total cholesterol or high levels of triglycerides)
Liver and Gallbladder disease
Sleep apnea and respiratory problems
Osteoarthritis (a degeneration of cartilage and its underlying bone within a joint)
Gynecological problems (abnormal menses, infertility)


Prior to the 20th century, obesity was rare. The WHO in 2005 estimated that at least 400 million adults worldwide (10%) were obese. WHO predicts that obesity will overtake malnutrition and infectious disease as the most significant cause of poor health. Obesity rates are rising even among poorer, developing countries.

It is estimated that in 2010, Americans spent $60.9 billion on weight loss. In 1998, medical costs due to obesity in the US were $78.5 billion. Obese workers had higher rates of absenteeism and disability leaves. This increases the cost for employers while receiving decreased productivity. Therefore, obese people are less likely to be hired for a job and receive fewer promotions. Obese children are frequent targets of bullies.

A fat acceptance movement has started with organizations like National Association to Advance Fat Acceptance and International Size Acceptance Association. However, obesity has not yet received the same type of support as the civil rights movement.

Benefit of weight loss

The Framingham heart study shows that weight loss resulted in lower blood pressure and lipid profiles. Studies have shown up to a 20% reduction in mortality due to weight loss. Risk is lowered in obese patients with hypertension, dyslipidemia, and diabetes.

Anti-obesity medications attempt to alter appetite, metabolism, or absorption of calories. Due to the side effects and addiction profile of some drugs, medications should be individualized and prescribed when the risk of obesity outweighs the potential risks of the drugs.

hCG Diet overview by Dr. Jay Park MD

Medications Used in Medical Weight Loss

Weight-loss attempts are described as far back as the 2nd century AD, where a Greek physician prescribed laxatives, along with heat, massage, and exercise. In the 1920s thyroid hormone was used on obese patients with some effects, but they also had hyperthyroidism as a side effect. Dinitrophenol was introduced in 1933, which uncoupled oxidative phosphorylation in the mitochondria to produce heat instead of ATP. This was discontinued due to side effects including fatal hyperthermia. Amphetamine was also used in the 1930s, which was later banned by the FDA due to an increasing number of deaths. Fen-phen was approved in 1959, but in 1997 was removed due to evidence that it causes valvular heart disease. Ephedra was another stimulant that was subsequently removed from the US market due to concern of strokes and deaths.

It is important to treat obesity as a chronic disease without a cure. Currently, no safe or effective treatment exists for rapid and long term weight loss. Most experts recommend losing 1 to 2 pounds per week. Behavioral therapy, exercise and dietary modifications are the three main pillars of successful weight loss maintenance. However, the rate of relapse back into obesity is high. Therefore, various pharmacologic options are used as adjuncts to traditional weight loss programs.

Finally, there are many off-label uses of drugs (Synthroid, metformin, Prozac, etc.) that physicians use to treat obesity. Most of these drugs are not included in this presentation as they lack good clinical evidence of significant results.

Typically, anyone with any of the following symptoms should be excluded from using pharmaceutical agents: severe systemic illnesses, psychiatric illness, hypertension, cardiac disease, pregnancy, breastfeeding, aged under 18 or above 50, and any drug to drug interactions.

We will review the most basic types of medications to start for your patient in this medical weight loss training certification manual.

Appetite Suppressants

Two classes of anorectic drugs are currently available: noradrenergic and the serotonergic agents. Norephinephrine, serotonin and dopamine are neurotransmitters in the hypothalamus (the appetite center), which is thought to play a role in energy intake, energy expenditure, substrate utilization, and adipose storage.

Noradrenergic Agents

Phentermine is the most commonly prescribed appetite suppressant currently in the US market. Fen-Phen was a drug that combined fenfluramine with phentermine. This drug was pulled from the US market due to it causing valvular heart disease. Phentermine continues to be sold as a single weight loss agent. Phentermine is structurally similar to amphetamine, which makes it a DEA schedule IV drug, and affects the noradrenergic neurotransmission.

In clinical trials, the use of phentermine alone resulted in significant weight loss when compared with placebo. At the end of 36 weeks, 13% weight loss was achieved.

The typical dose ranges from 30mg to 37.5mg per day. Typically, usage should be limited to a maximum of 8 to 12 weeks, as many studies show a tolerance. Another study looked at intermittent dosing, one month on and one month off, and saw that the intermittent treatment was just as effective. Typically, the patient will start off with half of the 37.5mg tablet, once per day in the morning before breakfast. Patients can take a half tablet in the evening if night appetite suppression is needed (insomnia can become a problem). Patients can increase to one whole tablet in the morning if tolerance is reached.

The most common side effects include insomnia, dry mouth, heartburn, decreased sex drive, headache, nervousness, and irritability. Palpitations, tachycardia, and hypertension may occur. Phentermine should not be taken by persons with symptomatic cardiovascular disease, moderate to severe hypertension hyperthyroidism, glaucoma, agitated states, advanced arteriosclerosis, or a history of drug abuse. Please see the package insert for full description.

Diethylpropion is another noradrenergic appetite suppressant that is used. The mechanism of action and side effect profile is similar to phentermine. The starting dose is 25mg three times a day, before meals for up to 8 to 12 weeks. In a clinical trial, diethylpropion at 75mg per day, after 6 months, patients saw a 12.3% body weight loss vs placebo (2.8%).

Serotonergic Agents

The serotonergic drugs act on the hypothalamus to decrease satiety by partially inhibiting the reuptake of serotonin and release serotonin into the synaptic cleft.

Fluoxetine (Prozac) was thought to be a promising solution to obesity, but weight loss has not been consistent among subjects in clinical trials. A three-month study failed to show benefit over placebo. However, at 20 weeks, significantly greater weight loss was achieved. Unfortunately, after one year, weight loss between the two groups was not different. Fluoxetine continues to be used by some physicians as an off label use.

Adrenergic/Serotonergic Agents

Sibutramine (Meridia) is an adrenergic/serotonergic agent approved by the FDA in 1997 for use in the management of obesity. Initially tested as an antidepressant, patients in the sibutramine group lost weight that was dose-dependent. Sibutramine inhibits monoamine uptake, suppressing appetite in a fashion similar to SSRIs. Also, sibutramine may also stimulate thermogenesis by activating the beta3-system in adipose tissue. It does not stimulate the secretion of serotonin.

Sibutramine has been withdrawn from the market due to low efficacy and raised risk of heart attack and stroke.

Phen-pro (phentermine 30mg –Prozac 20mg) is another combination drug that is used off-label for weight loss. Similar to sibutramine, it is believed that phen-pro causes increased norephinephrine and serotonin activity in the hypothalamus to reduce hunger. However, this combination is poorly studied and lacks good medical research to be recommended.

Thermogenic Agents

There is no drug that is available in the US market currently. However, combination ephedrine and caffeine exists, which has anorectic and thermogenic properties. Ephedrine causes the release of norepinephrine, which affects food intake, and enhance thermogenesis. Caffeine, an adenosine antagonist, reduces the breakdown of norepinephrine within the synaptic junction, which enhances the effects of ephedrine. Studies showed that ephedrine (20 mg) with caffeine (200 mg or two to three cups of caffeinated coffee) taken three times daily was found to be more effective than placebo or either drug alone. Side effects, such as tremors, insomnia, and dizziness, were transient after eight weeks of treatment and compared with placebo effects. Although clinically effective, the risk of cardiac complications limits it clinical use.

Thyroid hormone also increases the metabolic rate, but it causes unwanted side effects such as tachycardia and is associated with increased protein loss. It has not been recommended as a weight loss medication, because its effect on weight loss is minimal.

Digestive Inhibitors

Orlistat (Xenical), the first lipase inhibitor approved by the FDA in 1998 for the treatment of obesity, is an irreversible inhibitor of gastric and pancreatic lipases and prevents the absorption of 30 percent of fat. Orlistat inhibits enzymes from breaking down triglycerides into free fatty acids. Therefore, triglycerides, cholesterol, and lipid-soluble vitamins are poorly absorbed and excreted in the feces.

Orlistat is approved for patients with a BMI of at least 30 kg per m2 or in patients with hypertension, diabetes or dyslipidemia with a BMI of greater than 27 kg per m2

In a one-year double-blind, placebo-controlled study, weight loss ranged from 3 to 4 kg (6.6 to 8.8 lb) with 120mg of orlistat three times a day versus placebo. Patients regained about 2 kg (4.4 lb) during the second year of orlistat versus placebo. Studies have also shown weight loss of 8.5 percent at one year compared with 5.4 percent for placebo Improvements in blood pressure, cholesterol levels, glucose and insulin measurements were recorded, but the difference was not clinically significant.

Side effects include flatus, steatorrhea, fecal incontinence, and oily spotting. These effects are more significant in patients eating a high-fat diet. Changes in coagulation parameters in patients being treated with warfarin (Coumadin) occur, because of decreased vitamin K absorption. One study showed that concentrations of fat-soluble vitamins were lower in orlistat patients than in the placebo group, but the numbers remained within the reference range. Also, in 2010, FDA issued a warning about severe liver injuries related to orlistat.


Metformin has been shown to result in weight loss in diabetics and patients with polycystic ovary syndrome. A meta-analysis showed that only 2 of the 9 studies showed a small reduction in the waist to hip ratio. They concluded that “insufficient evidence exists for the use of metformin as treatment of overweight or obese adults who do not have diabetes mellitus or polycystic ovary syndrome.”

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