By Paula Hendricks - Nutritionist on March 3, 2010
PRODUCTS & SPECIALS
FROM THE DOCTOR – Ed J. Hendricks, M.D.
What’s all the talk about the latest diet craze using HCG? Maybe a friend has told you about it or you read about it somewhere. What is it and does it help with weight loss?
HCG, Human Chorionic Gonadotropin, is a hormone produced by the placenta during pregnancy, and is not the latest, greatest weight loss product on the market today. In fact, it was first introduced for weight loss by Dr. A. Simeons back in 1954, who believed that the HCG hormone accelerated weight loss and suppressed hunger. He combined daily injections of HCG with a prescribed diet – a diet now known to be dangerously low in protein intake. This nutrient poor diet was actually a starvation diet. While it is true starvation diets produce rapid weight loss, much of what is lost is muscle – not a healthy way to lose weight.
The Simeons method was wildly popular in California in the 1970s until several clinical trials proved that HCG had nothing to do with the weight loss. Although only a few clinics in the metropolitan Sacramento area seem to be using HCG for weight loss today, in other parts of the country, HCG is becoming extremely popular again. Some of you have asked us if we will carry HCG. My answer. Absolutely not.
The HCG method is a hoax, a dangerous one. We strongly advise against using HCG, in any form, for weight loss and are especially critical of the diet used in combination with the HCG. If you want to know more detail about HCG, read the blog I posted on our website, hendricksforhealth.com, dated December 20, 2009, titled “HCG Treatment for Obesity – HCG and Weight Loss,” or pick up a copy in the office at your next visit.
FROM THE NUTRITIONIST – Paula Hendricks, BS, Nutritionist-C
Recipes and Hand-outs:
By Paula Hendricks - Nutritionist on March 3, 2010
Crab Cakes with Greens and Sauce– Makes 4 Servings
If you thought traditional crab cakes were not on your diet menu, you were right – too many bread crumbs and too much fat. Good news though…I have created a crab cake recipe that you can make yourself without deviating from your weight loss and health goals. They are pretty simple to make and fresh crab is easy to find in the refrigerated section of your local store. My family and friends have been enjoying my crab cake experiments this past month and with good feedback – I think I have it right now. Enjoy on all Key Diets.
Ingredients -
For the Crab Cakes:
For the Sauce:
Instructions:
Variations: Add minced red peppers, chives, or fennel for a different flavor. Substitute the cilantro for parsley or other spice. Reduce the fat by omitting the mayonnaise in the sauce. Don’t like pork rinds. Replace with low-carb bread crumbs or crackers (not for the VLCD).
Nutritional Value: Each serving contains approximately 265 calories, 32 grams of protein, 14 grams of fat and only 1 gram of carbohydrates.
By Paula Hendricks - Nutritionist on February 10, 2010
PRODUCTS & SPECIALS
FROM THE PRACTITIONER - Cheryl Mitchell, PA-C, MPAS
Everyone knows thin people have more willpower than overweight people – right?
Have you struggled to control your weight and overeating all your life (or alternatively – since you had kids, since menopause, since an injury – pick one)? Do you wish you had the self-control and willpower to stay thin like (insert name of your example here)? Do you wonder how you can change so you’re as strong as they are?
Let’s reframe the situation. Your has-always-been-thin person above never overeats. They know when they are full and stop eating. Stresses don’t make them hungry – so they eat only when they really need food. Their “appestat” (appetite thermostat) works like it should. Does their “appestat” drive them to eat when their body doesn’t need the food or nutrients? No! So how much willpower do they need to eat only what they need and not more? NONE! They have no desire to overeat. Control comes naturally; they would have to force themselves to overeat. Your has-always-been-thin person stays thin but says nothing about their willpower or strength – they don’t need any willpower to stay thin.
Now let us look at you and your need for willpower. You struggle every day, often all day to eat only what your body needs, but your brain is not satisfied. Your stomach is full, often uncomfortably so, but your mind still says “keep eating”. Sometimes you fight the desire for food successfully, and other times you just can’t stay away from the unneeded food. The desire to eat is there when you are stressed, when happy, when cold…You fight not to eat all the time. Most of the time you resist the urge, but when the urge overwhelms you – you (and it seems like the rest of the world) call yourself weak, and that you have no willpower! Your thin person needs NO willpower to not overeat. You struggle everyday to control your eating – and win much of the time. I ask you – who is showing strength? The person who is never tested, or the person who, while tested all the time, loses occasionally? Give yourself credit for your strength.
FROM THE NUTRITIONIST – Paula Hendricks, BS, Nutritionist-C
In the distant past, perhaps sixty years ago, a series of nutritional research studies were thought to indicate that saturated fat intake could raise LDL “bad” cholesterol levels which in turn were thought to elevate risk for heart disease and stroke. Although not everyone agreed with this interpretation, the notion that eating fat causes coronary heart disease took hold and has been dogma for many years. However, a new analysis recently released in the American Journal of Clinical Nutrition, which reviewed the combined results of over 21 studies regarding cholesterol intake and heart disease, found no clear evidence that higher intakes of saturated fat led to higher risks of heart disease and stroke. Wow, that’s pretty comforting information for steak lovers, right? Don’t expect all the “experts” to promote eating red meat and high fat dairy products right away.
So what do we think about this new analysis and how does it affect what we teach our patients? Well, it is not new information to us at all, as evidenced by 20 years of clinical observation within our own practice. We have known for a long time that sugar and other processed carbohydrates were the “bad guys” in the American Diet rather than fat. Consumption of sugar, high carbohydrate processed foods, non-nutritive foods and trans-fat are the real culprits.
We believe that to single out specific nutrients such as saturated fat and ignore the entire diet is a mistake. In the 80s, we were told not to eat fat, in the 90’s we were told not to eat protein, and today, we have told all who would listen not to eat “bad carbs.” Of course, if you look at the Food Pyramid recommended by the FDA today, you’ll see they recommend that you get the majority of your food from carbohydrates, including “bad carbs,” the processed ones. It is confusing at best.
We believe consuming a balanced combination of foods containing all the macronutrients (proteins, carbohydrates, and fats) – animal protein, vegetables, fruits, nuts, and good fats – will reduce your risk of heart disease, stroke and chronic illnesses, promote longevity, and reduce your risk of illness as you age. However, the balanced combination of food we recommend deviates significantly from the “balanced diet” recommended by the FDA. We believe the FDA food pyramid is an out of balance, protein-deficient, essential fatty acid-deficient, high carbohydrate eating style which if consumed long enough, will inevitably induce diabetes, obesity and a host of other chronic illnesses. Just remember when you eat, protein is “good,” fat is “good,” and carbs can be either “good” or “bad.” To stay healthy, we all should learn to recognize and eat the good carbohydrates (vegetables and fruits) and avoid the bad carbohydrates (sugars), processed.
Recipes and Hand-outs:
By Paula Hendricks - Nutritionist on February 10, 2010
Chicken Paillard with Wine & Mushroom Sauce – Makes 4 Servings
I just love to serve this simple yet elegant chicken dish to my family on a weeknight –they think I went to so much effort because it’s that good. Even the name sounds elegant. Paillard simply means chicken that is pounded with a mallet until very thin and grilled which, by the way, makes it very tender. The best part – it only takes about 15-20 minutes to prepare this dish from start to finish. Have a side salad ready. Enjoy on any of the Key Diets.
Ingredients:
Instructions:
1. Place two pieces of chicken breasts between two pieces of plastic wrap or in a plastic bag and pound chicken with the smooth side of a mallet (or use a small saucepan) until chicken is uniformly about 1/8-1/4 inch thick. Continue until all pieces have been pounded. Season with the poultry seasoning or seasoning of your choice.
2. Have all ingredients out, measured and ready to use before you start grilling. If using fresh mushrooms, put them in the microwave in a covered bowl on high for 2-3 minutes. Drain any excess liquid.
3. Heat a skillet over high heat (don’t use non-stick). Add one tablespoon olive oil to the pan and 4 pieces of the chicken. Grill on each side for about 1 ½-2 minutes – chicken should be slightly browned and cooked through. Place cooked chicken on a plate, cover and keep warm.
4. Cook second batch of chicken as directed above.
5. After chicken is cooked, in the same pan, turn heat down to medium and add the wine. Be careful as the wine will steam and bubble. With a wooden spoon, scrape the inside of the pan to dislodge any residual chicken bits to prepare the juice. Add the minced garlic and stir for another 30 seconds.
6. Add the chicken broth and lemon juice and wait for liquid to bubble, about 1 minute. Gradually add the sour cream and stir quickly with a whisk to blend. If not thick enough, add a little more sour cream, about 2 tablespoons. Turn down heat on pan to low and let simmer for about 1 minute.
7. Add the mushrooms and simmer for one more minute.
8. To assemble for serving, place two pieces of chicken on a dinner plate and top with a little mushroom wine sauce.
9. Garnish the plate with some fresh herbs, lemon wedges or toss some capers on top.
Variations: Don’t like mushrooms? Omit them and put chicken and sauce over sautéed spinach or chard.
Nutritional Value: Each serving contains approximately 270 calories, 35 grams of protein, 10 grams of fat and 9 grams of carbohydrates.
By Dr. Ed Hendricks on January 21, 2010
Does phentermine induce or provoke relapse of substance abuse?
Statement of the Issue: FDA drug labeling and the PDR state that phentermine is contraindicated in patients with a history of drug abuse. The FDA’s hypothesis is that phentermine, a category IV controlled substance, prescribed for such patients can provoke relapse of drug abuse (first hypothesis). A corollary hypothesis, which must also be true for the first hypothesis and the FDA’s contraindication to be valid, is that phentermine has significant human addiction potential (second hypothesis).
Origin of the Issue & Historical perspective: Phentermine was approved for marketing by the FDA in 1959. At the time phentermine was approved, far less was understood of the nature of stimulant drug abuse than is the case today. At that time, the favored hypothesis was that stimulant abuse potential was directly correlated to stimulant potency. No suggestion of abuse or dependence had appeared in any of the clinical trials conducted prior to approval. However, a series of animal studies in rats beginning in the 1950s and continued into the 1960s which examined changes in spontaneous activity showed that phentermine increased spontaneous activity more than placebo.(1) Even though there was complete absence of clinical evidence in humans, the FDA relied on the animal data, and assuming stimulation in rats equated to abuse potential in humans, classified phentermine as a category IV controlled substance. In reading the FDA labeling in the 2010 edition of the PDR, which differs from the original 1959 labeling in only a few details, it is clear that the FDA has always assumed that phentermine has exactly the same risks and adverse effects as amphetamine.
In 1959 commonly agreed upon criteria for diagnosis of drug abuse, dependence and addiction had not been established. The first edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-I), published in 1952 listed drug addiction as a diagnosis but neither discussed nor provided criteria for the diagnosis. Several drugs of addiction were listed but amphetamine was not included; indeed the nature of amphetamine abuse, addiction, and withdrawal was poorly understood in 1959. At that time modern addiction medicine methodology and psychometric testing were in their infancy and there were no standardized examination techniques for addiction.
After the 1962 passage of Kefauver-Harris amendments to the Food, Drug and Cosmetics Act, the FDA reevaluated the anorectic drugs. For ten years thereafter, as the FDA continued the re-evaluation the major perceived risk of the anorectics was addiction. Although the amphetamines clearly posed a risk of addiction, the addictive potential of the amphetamine congeners had not been thoroughly studied in humans and remained open to debate. Based on structural similarities and some anecdotal evidence some of the expert panel considering the drugs believed that phentermine also had a risk for abuse and addiction. Eventually in 1973 a compromise was reached in the debate and the anorectic drugs including phentermine were re-approved with the proviso that the labeling restrict use to a few weeks and that the drugs be prominently labeled to warn about the risk of addiction.(2)
Currently, as a result of numerous investigations into the nature of substance abuse, addiction medicine specialists have developed clearly defined criteria for substance abuse disorders. These criteria did not exist in 1959 when phentermine was approved, or in 1973 when the FDA debate was “settled” reaffirming phentermine was addicting and only emerged with the publication of the DSM-IV in 2000. The term “addiction” has been replaced with “dependence” and “abuse.” Substance dependence is defined as a maladaptive pattern of substance use, leading to clinically significant impairment or distress, as manifested by three (or more) of the following, occurring at any time in the same 12-month period:
1) Tolerance – markedly increased amounts needed.
2) Withdrawal – syndrome characteristic for the substance.
3) Substance taken in higher amounts or for longer duration than intended.
4) Persistent desire or unsuccessful attempts to cut down or control use.
5) A great deal of time spent in obtaining the substance (e.g. seeing multiple doctors, driving long distances), using the substance, or recovering from its effects.
6) Important activities are given up or reduced because of substance use.
7) Substance use is continued in the face of significant social, family, occupational, or legal problems caused or exacerbated by use.
Substance abuse is defined as a maladaptive pattern of substance use, leading to clinically significant impairment or distress, as manifested by one (or more) of the following, occurring at any time in the same 12-month period:
1) Recurrent use resulting in failure to fulfill major role obligations at work, school or home.
2) Recurrent use in situations where it is physically hazardous.
3) Recurrent use-related legal problems.
4) Continued use despite persistent social or inter-personal problems.
A diagnosis of substance dependence is of greater severity than substance abuse. Substance abuse should not be diagnosed in any patient with a prior diagnosis of dependence. Patients who have substance dependence who abruptly cease taking the substance develop a withdrawal syndrome characteristic of the substance involved. Intense cravings for the substance are a cardinal feature of substance dependence and withdrawal.(3)
The substances of abuse have been classified into categories; amphetamines are classified as stimulants with cocaine being the prototypical stimulant of abuse. Addiction medicine specialists have also developed psychometric tests for the diagnosis and severity assessment of substance abuse disorders.(3-7) Psychometric tests have recently been used to accurately describe the features of amphetamine abuse, dependence and withdrawal.(8-10)
Currently the only investigation in the peer-reviewed medical literature (in press) which has examined the addiction potential of phentermine using modern addiction medicine methodology is the one we recently did in this practice.(11)
Methods Used for Evidence Searches: The National Library of Medicine currently catalogues every paper published in the peer reviewed medical literature. PubMed, the NLM search engine, now has 19,000,000 articles catalogued and accessible online. Papers as far back as 1928 are included. Every reference in this memo is catalogued there. Any bibliographies developed using PubMed search algorithms may be stored in a personal account with automatic email notification when new papers are added to the bibliography. The result is that anyone, anywhere in the world, has instant access to the resources of the National Library of Medicine.
Evidence for the two hypotheses: There is no evidence in the peer-reviewed medical literature which supports the first hypothesis that phentermine therapy can provoke relapse in patients with a history of substance abuse. Indeed, there is little in the literature to support the second hypothesis that phentermine has addiction potential in humans. On the other hand, many textbooks repeat the FDA conjectures but none of these offer any supporting evidence or cite supporting peer-reviewed literature other than animal studies, primarily in rodents, measuring stimulant activity or self-administration data. More recent animal studies in primates do not support the notion that phentermine has addictive potential.(12) In fact, in studies in rhesus monkeys, phentermine is effective in decreasing cocaine self-administration suggesting it may be a useful drug in treating cocaine addiction.(13-14)
PubMed searches, limited to humans and excluding animal studies, for “phentermine AND abuse,” “phentermine AND dependence,” “phentermine AND withdrawal,” found only one anecdotal report of phentermine addiction, which predated the publication of diagnostic criteria for dependence, abuse, and withdrawal.(15) These searches found a few other papers, reviews focused on drug safety, which discussed phentermine but included no data.(16-17)
The studies the FDA has relied upon in asserting both hypotheses must be considered indirect evidence since the studies were all animal studies. Thus it seems that although it is “common knowledge” that phentermine is addicting, direct evidence in support of this knowledge is nowhere to be found. The few papers that exist which might support the addiction potential hypothesis in human subjects are anecdotal.(18-19)
Evidence against the two hypotheses:
1. There have been numerous phentermine clinical trials reported in the peer-reviewed medical literature most which have been re-examined several times in meta-analyses.(20-24) Adverse side effects were monitored in each trial. There were no signs of abuse, dependence or withdrawal reported in any of the clinical trials. This is direct evidence contradicting the second hypothesis.
2. A recent investigation, conducted in the author’s practice, of the addiction potential of phentermine involved studying symptoms occurring in patients in a medical weight loss program who abruptly ceased taking phentermine after having been on long-term phentermine pharmacotherapy. If phentermine does indeed have addictive properties, one would expect that such patients would experience symptoms similar to those seen in amphetamine addicts when such subjects abruptly cease amphetamine use at a treatment center. Amphetamine cessation in addicts has been studied and psychometric scales devised to assess withdrawal severity.(25) The study found that long-term phentermine pharmacotherapy in the context of a weight management program did not induce amphetamine-like withdrawal symptoms. The study also indicated that long-term phentermine pharmacotherapy did not induce phentermine cravings in any degree. This was true even in patients who had been on phentermine therapy for as long as eleven years and in patients on doses higher than recommended in the package insert.(11, 26)
This report of symptoms following abrupt phentermine cessation is direct evidence that phentermine has little or no addiction potential; direct evidence in human subjects contradicting the second hypothesis.
3. The fact that phentermine pharmacotherapy does not induce cravings for phentermine is highly significant since intense cravings for the substance are cardinal features of substance dependence and withdrawal. The author, in another on-going study, not as yet published, is assessing cravings using the Tiffany Cocaine Craving Questionnaire(27) modified for phentermine and has found that phentermine treated subjects do not develop phentermine cravings. This too is direct evidence that the second hypothesis is not true.
4. Attention Deficit Disorder is typically treated with amphetamine drugs, category II controlled substances. There has been concern that treatment with category II drugs might induce substance abuse in treated subjects. Wilens and colleagues at Massachusetts General Hospital and Harvard Medical School has studied this question extensively and has concluded that, contrary to expectations, patients treated with amphetamine have a lower, not higher, incidence of drug abuse when compared to untreated patients.(28-33)
Given these the results of these studies in amphetamine, a drug known to much more potent than phentermine in stimulant strength and in creating adverse side effects, it seems unlikely that the first hypothesis is correct for phentermine, a category IV drug. It is true that this is indirect evidence, but it seems compelling never-the-less. If amphetamine therapy produces a decrease in incidence of substance abuse, how could the weaker drug, phentermine, produce an increase in substance abuse? These studies in ADD patients provide indirect evidence contradicting the first hypothesis.
5. Some of the acknowledged experts in obesity treatment have commented in published reviews that if phentermine indeed has addiction potential, it is vanishingly low and has not been a problem in clinical practice.(34-36) The author of another report discussing long-term phentermine use (more than ten years) noted that he had not observed abuse or dependence even in patients who had been on phentermine as long as 40 years.(37)
This too is indirect evidence against the second hypothesis. Even though this is indirect evidence I would argue clinical observations by experts with long experience with phentermine should be more convincing than studies in rodents.
6. My own experience has been that a prior history of drug abuse is not an absolute contraindication to phentermine. Patients who are currently abusing or are addicted to substances do not often present themselves to a physician for weight loss – they are too preoccupied with their addiction to be concerned with being overweight. Stimulant addicts typically select much stronger stimulants than phentermine as their drug of choice. Cocaine, methamphetamine, and amphetamine are likely choices. Phentermine may be abused by stimulant addicts in desperation if their drug of choice isn’t available to them or phentermine may be added to a cocktail of a variety of compounds in an attempt to achieve a stronger stimulant mix. Although one old report from a methadone treatment program indicated that 22% of urine samples from their patients contained traces of phentermine,(18) recent informal surveys of drug treatment centers indicate that phentermine abuse or dependence is not seen or treated at such centers today. I have not encountered a patient currently addicted to stimulants in 20 years of practicing bariatric medicine in a busy weight loss clinic.
Patients with a prior history of substance abuse who are currently abstinent do present themselves for weight loss. Some of these never admit their prior abuse to the physician. Some patients do reveal their past experience after varying intervals of treatment. My experience has been that when these patients are treated with phentermine they never have a return of cravings for the substance they once abused even when the substance was amphetamine, or the potently addicting amphetamine congeners such as methamphetamine, crystal methamphetamine, or 3,4-methylenedioxymethamphetamine (MDMA or “ecstasy”).
I have treated perhaps two dozen such patients with phentermine who have at first denied prior substance abuse or dependence. As these patients have confessed to a prior substance disorder I have quizzed them for signs or re-emergence of cravings for the previous substance and for phentermine. If there are no such symptoms, I continue phentermine pharmacotherapy. These patients have not developed phentermine-induced substance abuse nor have they relapsed into substance abuse or dependence.
The fact that some patients at first deny prior illicit drug abuse suggests that an unknown number of patients, unsuspected of being former addicts, are unwittingly treated with phentermine in weight loss practices across the U.S. The fact that this practice has never emerged as a problem is also compelling indirect evidence that the first hypothesis cannot be true.
In my experience, phentermine does not provoke or induce cravings for either phentermine or substances of abuse. Patients who admit to prior substance abuse, dependence or withdrawal can be treated with phentermine provided the treating physician is convinced that the patient is trustworthy, but this must be done with care and caution. When phentermine treatment is undertaken the physician must continuously be watchful for the emergence of cravings for other drugs and for drug seeking behavior; should these appear, phentermine should be discontinued. The patient should be informed that phentermine pharmacotherapy for anyone with prior substance disorders is controversial and if the patient chooses to discontinue phentermine the patient’s wishes should be respected.
My experience is anecdotal and therefore must be considered indirect evidence contrary to the second hypothesis. The fact that not a single instance has been reported in which phentermine therapy provoked relapse of a substance abuse disorder must also be considered indirect evidence contrary to the first hypothesis.
7. The clinical features of the abuse, dependence, and withdrawal syndromes of the drugs of addiction are described in the DSM-IV. Although the syndromes for stimulants of abuse are described including cocaine, amphetamine, methamphetamine, methylphenidate, and others, the DSM-IV does not mention phentermine. In fact, no syndromes of abuse, dependence or withdrawal for phentermine have ever been described even though it has been widely available for 50 years. This is another piece of indirect evidence contradicting the second hypothesis.
8. One final point is that, after 50 years of widespread use, the absence of published evidence in support of the first hypothesis is indirect evidence that the hypothesis is false. The same is true of the second; after 50 years of use there are no credible reports of phentermine addiction providing indirect evidence the second hypothesis is false.
Discussion: The type and severity of adverse effects produced by any drug is influenced by the dose, route and duration of administration. Subjects who abuse amphetamine and other stimulants typically self-administer the drug by either the inhalational or intravenous route. These routes of administration typically produce very high plasma drug levels very quickly,(38) increasing the probability of producing serious adverse effects, such as addiction. Patients taking oral stimulants, as prescribed by a physician, simply do not achieve the high plasma drug levels needed to produce serious adverse effects. This fact likely explains the overall very low rate of serious adverse effects seen with the use of stimulants for the treatment of obesity and also of attention deficit disorder.(39) Patients in weight management programs are typically seen often and prescribed only enough phentermine to last until the next visit. The fact that they do not self-administer the drug by inhalation or injection is an important aspect of the question of the addiction potential of phentermine – one that has been completely ignored in the controversy. The addiction potential of phentermine must be examined within the context of a weight management program – whether or not substance abusers might add it to a stimulant cocktail should not be part of the argument.
Summary: The existing evidence regarding the two hypotheses is summarized in Table 1 and Table 2 on the following page.
Table 1. Summary of Evidence
First Hypothesis: Phentermine given to a patient with prior substance abuse will provoke relapse of drug abuse
| Evidence
For/against |
Evidence type | Evidence | Published Literature |
| FOR | Direct | None | No |
| Indirect | None | No | |
| AGAINST | Direct | None | No |
| Indirect | Attention Deficit Disorder patients treated with amphetamines have lower incidence of substance abuse than do untreated ADD patients | Yes | |
| Indirect | No reported instances of phentermine treatment provoking relapse of substance abuse | No | |
| Indirect | Not seen in clinical experience | No |
Table 2. Summary of Evidence
Second Hypothesis: Phentermine has significant human addiction potential.
| Evidence For/Against | Evidence Type | Evidence | Published Literature |
| FOR | Direct | None | No |
| Indirect | Older animal studies, 1950 to ~1980 | Yes | |
| AGAINST | Direct | Multiple human clinical trials, 1975 -2006 | Yes |
| Direct | Abrupt Phentermine Cessation Study, 2010 | Yes | |
| Direct | Long-term Phentermine Rx does not induce phentermine cravings, no matter dose or duration, 2010 | Yes | |
| Indirect | Modern animal studies | Yes | |
| Indirect | Not seen in anyone’s clinical experience | Yes | |
| Indirect | No credible reports of human addiction | No |
Note that that there is absolutely no evidence, direct or indirect, to support the first hypothesis! The FDA admonition that prior substance abuse contradicts phentermine therapy is pure conjecture; no evidence supports the conjecture.
Conclusions: Phentermine pharmacotherapy for obesity does not provoke substance abuse in patients with prior substance abuse. Nor does phentermine induce substance abuse in patients with no prior history of substance abuse. Phentermine pharmacotherapy for obesity does not induce phentermine substance abuse. The existing evidence does not support either hypothesis. The first hypothesis is unproven and is therefore false. The second hypothesis is unproven and is therefore false.
Why hasn’t the FDA changed the labeling? The FDA will never change phentermine labeling until compelled to do so. A more cogent question then is “what must happen before the FDA will consider changing phentermine labeling?” The answer: at least three things.
First: More modern investigations into the human addiction potential of phentermine must be undertaken and published. More primate studies are needed as well. The preponderance of evidence the FDA has relied upon is evidence from older animal studies. Until the preponderance of evidence, both animal and human, clearly contradicts the second hypothesis, the FDA will not act.
Second: At least one large scale, long-term, randomized, double blinded phentermine trial which satisfies current FDA Guidance must be undertaken and published. My understanding is that a group of investigators recently applied for a NIH grant to do this only to have the application rejected (personal communication, K.M Gadde, October 2009). The group is preparing to re-apply. Because phentermine is widely used as the agent of choice obesity treatment, a long-term trial investigating effectiveness and safety is in the public interest and should be undertaken. This is the major critical requirement which must be satisfied before the FDA will act. A large scale prospective trial designed to test the first hypothesis would be a difficult undertaking but is also needed.
Third: The FDA must be presented with a petition to asking that phentermine labeling be changed. This should not be undertaken until the first two requirements are satisfied; otherwise the FDA will undoubtedly reject the petition.
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26. Hendricks EJ, Greenway FL. A study of abrupt phentermine cessation in patients in a weight management program. American Journal of Therapeutics 2010, In Press, Manuscript AJT-20082603.
27. Tiffany ST, Singleton E, Haertzen CA, et al. The development of a cocaine craving questionnaire. Drug and alcohol dependence 1993, 34 (1), 19-28.
28. Biederman J, Monuteaux MC, Spencer T, et al. Do stimulants protect against psychiatric disorders in youth with adhd? A 10-year follow-up study. Pediatrics 2009, 124 (1), 71-78.
29. Biederman J, Spencer TJ, Wilens TE, et al. Long-term safety and effectiveness of mixed amphetamine salts extended release in adults with adhd. CNS Spectr 2005, 10 (12 Suppl 20), 16-25.
30. Wilens TE. Attention deficit hyperactivity disorder and substance use disorders. Am J Psychiatry 2006, 163 (12), 2059-2063.
31. Wilens TE, Adamson J, Monuteaux MC, et al. Effect of prior stimulant treatment for attention-deficit/hyperactivity disorder on subsequent risk for cigarette smoking and alcohol and drug use disorders in adolescents. Arch Pediatr Adolesc Med 2008, 162 (10), 916-921.
32. Wilens TE, Adamson J, Sgambati S, et al. Do individuals with adhd self-medicate with cigarettes and substances of abuse? Results from a controlled family study of adhd. Am J Addict 2007, 16 Suppl 1 14-21; quiz 22-13.
33. Wilens TE, Faraone SV, Biederman J, et al. Does stimulant therapy of attention-deficit/hyperactivity disorder beget later substance abuse? A meta-analytic review of the literature. Pediatrics 2003, 111 (1), 179-185.
34. Pi-Sunyer FX. Use of lifestyle changes treatment plans and drug therapy in controlling cardiovascular and metabolic risk factors. Obesity 2006, 14 (suppl_3), 135S-142.
35. Bray GA, Greenway FL. Current and potential drugs for treatment of obesity. Endocr Rev 1999, 20 (6), 805-875.
36. Bray GA. Use and abuse of appetite-suppressant drugs in the treatment of obesity. Ann Intern Med 1993, 119 (7_Part_2), 707-713.
37. Frank A. The long-term management of obesity with continuing pharmacotherapy. Obes Res 2004, 12 (11), 1821-1827.
38. Evans SM,Cone EJ, Henningfield JE. Arterial and venous cocaine plasma concentrations in humans: Relationship to route of administration, cardiovascular effects and subjective effects. The Journal of pharmacology and experimental therapeutics 1996, 279 (3), 1345-1356.
39. Rothman RB, Hendricks EJ. Phentermine cardiovascular safety. American Journal of Emergency Medicine 2009, 27 1010-1013.
By Paula Hendricks - Nutritionist on January 6, 2010
PRODUCTS & SPECIALS
FROM THE DOCTOR
Happy New Year! Thank you again for celebrating with us 20 years of helping people get healthy by making positive changes in their lives through nutrition, physical fitness, and the right mindset. As we enter our 21st year, we will continue to offer the best medical care, share the latest medical research in nutrition and caring for the overweight individual, and continue to guide you with your goals for health and wellness. I look forward to seeing you in the office soon.
FROM THE NUTRITIONIST
It’s time! Get your mind right, refocused and ready to start the New Year on the right path. If you’re ready to jump right in, schedule an appointment today, set some goals, and get started. If you’re not ready to get fully started or commit, that is OK too. You are always welcome to come in for a no charge weigh-in and purchase some products to slowly ease back on track. We are here when you are ready. In the meantime, download a copy of the recipe of the month and the latest information about “Think 30!’ Not age, but grams of protein.
By Paula Hendricks - Nutritionist on January 6, 2010
Hearty Ham Soup – Makes Approximately Seven 2-1/2 Cup Servings
Warm yourself this January with this delicious, healthy and easy-to prepare soup. It is also very cost effective - hams are very inexpensive at most grocery stores right now. You can serve a large family, a small one with lots of leftovers, or a gathering for the Superbowl. Enjoy!
Ingredients:
Instructions:
1. If you have a slow cooker, I recommend using it for this recipe. Put all ingredients in cooker in the morning, except for lemon and heavy cream.
2. Let ingredients cook for up to 8 hours.
3. After it has cooked, remove two cups of soup, including vegetables and meat, place in blender and puree. Put ingredients back in cooker. This will thicken the base.
4. Add heavy cream and lemon juice. Stir.
5. Let cook on low for about another half hour. Add some water hot water if more liquid is needed, about one cup.
6. When ready to serve, use a measuring cup to visualize a 2 ½ cup serving. For each serving, put a blend of juice, meat and vegetables into each bowl to get a balanced meal.
Variations: Don’t like ham? Use chicken. Want to reduce your carbohydrate intake? Eliminate or half the amount of hominy in recipe. Don’t like heavy cream? Use some Cream of Celery condensed soup.
Nutritional Value: Each 2 ½ cup serving contains approximately 30 grams of protein, 12 grams of fat, 19 grams of net carbohydrates, and for those of you who must know the caloric count, 310 calories.
By Dr. Ed Hendricks on December 22, 2009
Arena Pharmaceuticals announced today that the company has submitted their application to the US Food and Drug Administration (FDA) for marketing approval for Lorcaserin, Arena’s internally discovered and developed drug candidate for weight management, including weight loss and maintenance of weight loss. The press release indicated the submission is based on an extensive data package from lorcaserin’s clinical development program that includes 18 clinical trials totaling 8,576 patients.
Now the waiting begins to see if the FDA will approve this novel drug.
By Dr. Ed Hendricks on December 20, 2009
History
Human Chorionic Gonadotropin (HCG) is a hormone normally secreted by the trophoblastic cells of the placenta during pregnancy. It was first described as a treatment for obesity in conjunction with a very low calorie diet by Dr. A. Simeons in 1954 [1]. The Simeons method consisted of a rigid diet of about 500 calories per day combined with 125 units of HCG injected six days per week for 8 weeks. For each of the two meals permitted daily, patients were instructed to select one item from each of four food groups, protein, vegetable, bread, and fruit. For protein servings patients were told to select from the following list: 3.5 ounces of meat, 3.75 ounces of fish, 4 ounces of Hoop cheese, or 6 egg whites. The latter two choices were to be selected occasionally [2]. The protein intake on the Simeons diet therefore ranged from about 45 to 50 grams per day. The Simeons method was very popular in the 1970s and advocates claimed that the method had numerous advantages including rapid weight loss with minimal hunger, no weakness, and dramatic loss of fat in the stomach, hips, thighs, and upper arms.
The method was wildly popular in the early 1970s; there were HCG weight loss clinics in every city in the U.S. After a series of clinical trials disputing the effectiveness of the Simeons method it fell from favor, but popular demand for HCG in the treatment of obesity has recently resurfaced in the United States. At the time the Simeons method was popular only HCG for injection was available. Sublingual HCG tablets were developed relatively recently. Perhaps this is one reason the method has resurfaced.
Discussion
Although there were a few early studies in agreement with Simeons recommendations [2-3], a number of subsequent studies produced evidence that the HCG in the Simeons method was ineffectual and that the weight loss was entirely due to the diet [4-7]. A meta-analysis review in 1995 of prior studies concluded that there is no scientific evidence that HCG is effective in the treatment of obesity [8]. The meta-analysis found insufficient evidence supporting the claims that HCG is effective in altering fat-distribution, hunger reduction or in inducing a feeling of well-being. The authors stated “…the use of HCG should be regarded as an inappropriate therapy for weight reduction…” In the authors’opinion, “Pharmacists and physicians should be alert on the use of HCG for Simeons therapy. The results of this meta-analysis supports a firm standpoint against this improper indication. Restraints on physicians practicing this therapy can be based on our findings.” PubMed and Google Scholar searches (on December 2, 2009) revealed no favorable reports on the Simeons method since the 1966 report by Lebon [3].
The diet employed in the Simeons method provides a daily protein intake below that recommended by the RDA for most patients. Although the caloric intake of the Simeons diet is similar to that of an early (prior to about 1985) VLCD, but the protein intake is much lower than that prescribed for VLCDs in current use. Indeed, in the last few years several well-known researchers have produced very convincing evidence that most adults benefit from protein intakes well above the minimum RDA and intakes more than double the minimum RDA improve weight loss during caloric restriction diets [9-10]. A further criticism of the Simeons diet is that the amounts of protein per serving recommended do not reach 30 grams, the threshold dose required for initiation of muscle protein synthesis [11-14]. In view of these recent advances in nutrition science, the Simeons diet is severely deficient in protein.
Recent studies indicate that HCG injections in men, especially men with testosterone deficiency, can produce a slight gain in muscle mass, thought to be due to rises in testosterone levels [15]. The doses in the latter study were 250 units twice weekly. However, no studies have been reported of muscle mass changes in patients before and after weight loss with the Simeons method. Therefore one cannot assume that weight loss with the Simeons method will result in a net gain in muscle mass. Rather, loss of muscle mass can be expected. There are no reports in the medical literature regarding the effectiveness of sublingual HCG.
Summary:
Numerous clinical trials have shown HCG to be ineffectual in producing weight loss. HCG injections can induce a slight increase in muscle mass in androgen-deficient males. The daily protein intake in the Simeons diet is set at about 40% of what we advise with our diets. The last favorable report of the Simeons method was in 1966, 43 years ago, at a time when scientific knowledge of protein requirements was rudimentary. All of the medical reports since 1966 reject both the use of HCG and the protein-deficient Simenons diet. Patients who are treated with the Simeons method lose weight because the diet is a protein-deficient starvation diet in which the patient loses muscle mass. Neither HCG infections nor sublingual HCG accelerates weight loss. The Simeons method is harmful since it promotes loss of muscle mass.
Recommendations:
References:
1. Simeons A. The action of chorionic gonadotropin in the obese. Lancet 1954; 2: 946-947.
2. Asher WL, Harper HW. Effect of human chorionic gonadotrophin on weight loss, hunger, and feeling of well-being. Am J Clin Nutr 1973; 26: 211-218.
3. Lebon P. Treatment of overweight patients with gonadotropin: follow-up study. J Am Geriat Soc 1966; 14: 116-125.
4. Greenway FL, Bray GA. Human chorionic gonadotropin (HCG) in the treatment of obesity: a critical assessment of the Simeons method. West J Med 1977; 127: 461-463. PMCID: 1237915.
5. Stein M, Julis R, Peck C, Hinshaw W, Sawicki J, Deller J, Jr. Ineffectiveness of human chorionic gonadotropin in weight reduction: a double-blind study. Am J Clin Nutr 1976; 29: 940-948.
6. Young RL, Fuchs RJ, Woltjen MJ. Chorionic Gonadotropin in Weight Control: A Double-Blind Crossover Study. JAMA 1976; 236: 2495-2497.
7. Bosch B, Venter I, Stewart RI, Bertram SR. Human chorionic gonadotrophin and weight loss. A double-blind, placebo-controlled trial. S Afr Med J 1990; 77: 185-189.
8. Lijesen GK, Theeuwen I, Assendelft WJ, Van Der Wal G. The effect of human chorionic gonadotropin (HCG) in the treatment of obesity by means of the Simeons therapy: a criteria-based meta-analysis. British journal of clinical pharmacology 1995; 40: 237-243. PMCID: 1365103.
9. Layman D. Dietary guidelines should reflect new understandings about adult protein needs. Nutrition & metabolism 2009; 6: 12.
10. Layman DK. Protein quantity and quality at levels above the RDA improves adult weight loss. J Am Coll Nutr 2004; 23: 631S-636S.
11. Paddon-Jones D, Rasmussen BB. Dietary protein recommendations and the prevention of sarcopenia. Curr Opin Clin Nutr Metab Care 2009; 12: 86-90.
12. Paddon-Jones D, Short KR, Campbell WW, Volpi E, Wolfe RR. Role of dietary protein in the sarcopenia of aging. Am J Clin Nutr 2008; 87: 1562S-1566.
13. Paddon-Jones D, Westman E, Mattes RD, Wolfe RR, Astrup A, Westerterp-Plantenga M. Protein, weight management, and satiety. Am J Clin Nutr 2008; 87: 1558S-1561.
14. Symons TB, Sheffield-Moore M, Wolfe RR, Paddon-Jones D. A moderate serving of high-quality protein maximally stimulates skeletal muscle protein synthesis in young and elderly subjects. J Am Diet Assoc 2009; 109: 1582-1586.
15. Liu PY, Wishart SM, Handelsman DJ. A Double-Blind, Placebo-Controlled, Randomized Clinical Trial of Recombinant Human Chorionic Gonadotropin on Muscle Strength and Physical Function and Activity in Older Men with Partial Age-Related Androgen Deficiency. J Clin Endocrinol Metab 2002; 87: 3125-3135.
By Paula Hendricks - Nutritionist on December 4, 2009
PRODUCTS & SPECIALS
FROM THE DOCTOR You Want to Take my Blood Pressure Again?
Why so many? Beginning in November, the medical assistants have been taking 2-3 blood pressure readings per patient visit. Many of you are asking, “Why did we start doing this?” Well, there are several reasons. First, many patients are nervous when they first arrive at the office, and many have been rushing to make their appointment on time, or are anxious about their weigh-in. In these situations, the first blood pressure reading may be higher than normal. A second reading a few minutes later is often lower. Second, averaging two (or more) blood pressure readings is now the recommended standard of practice for measuring blood pressure in a physician’s office. Our own research has confirmed that a single blood pressure reading is sometimes inaccurate and misleading.
What do the blood pressure numbers mean and what should they be? The higher (systolic) number represents the pressure while the heart contracts to pump blood throughout the body. The lower number (diastolic) represents the pressure when the heart relaxes between beats. Review the chart below to determine your blood pressure category.
| BLOOD PRESSURE CATEGORY |
SYSTOLIC mmHg |
DIASTOLIC mmHg |
| Normal |
<120 |
<80 |
| Prehypertension |
120-139 |
80-89 |
| Hypertension, Stage 1 |
140-159 |
90-99 |
| Hypertension, Stage 2 |
≥160 |
≥100 |
Currently, the experts recommend lifestyle changes and/or weight loss as the only treatment for prehypertension. Patients with Stage 1 or Stage 2 hypertension are typically advised to make lifestyle changes, lose weight, and take anti-hypertensive medications. Untreated elevations in blood pressure are associated with higher mortality. It is now well-known that reducing blood pressure to normal levels extends life-span. This is the major reason a more accurate blood pressure measurement is important for your health.
What change should you expect with weight loss? If your blood pressure is above normal, you should begin to see a decrease in blood pressure with just a few pounds of weight loss. This is true even if you are already on medications to control hypertension. If your blood pressure is normal, less than 120/80 to begin with, you may see only a slight decrease in blood pressure. Of course if your blood pressure goes down with weight loss, it will go right back up if you regain the weight lost. An exercise program will also help to lower your blood pressure. Blood pressures for everyone tend to rise gradually as the years go by so if weight loss lowers your blood pressure, it may go back up with the passage of time even though you maintain your weight loss. If your blood pressure remains above normal, even with weight loss and exercise, we may recommend starting a blood pressure medication.
What about blood pressure medications? If you are on blood pressure medications, you may be able to reduce the dose or discontinue your medications entirely with weight loss. If you begin to experience lightheadedness or dizziness, it may mean your medication dosage should be adjusted. As with any medical concern, always discuss with your practitioner.
FROM THE NUTRITIONIST
Contact our non–surgical weight loss clinic, which serves Sacramento, Roseville, and surrounding areas, to schedule an appointment.
2310 Professional Dr., St. 200
Roseville, California 95661
Phone:916.773.1191
Fax: 916.773.0498
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2621 Capitol Ave.
Sacramento, California 95816
Phone: 916.551.1999
Fax: 916.551.1998
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