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.
References:
1. Rossum JMv, Simon F. Locomotor activity and anorexigenic action. Psychopharmacologia 1969, 14 248-254.
2. Colman E. Anorectics on trial: A half century of federal regulation of prescription appetite suppressants. Ann Intern Med 2005, 143 (5), 380-385.
3. Heinz AJ, Epstein DH, Schroeder JR, et al. Heroin and cocaine craving and use during treatment: Measurement validation and potential relationships. J Subst Abuse Treat 2006, 31 (4), 355-364.
4. Kampman KM, Volpicelli JR, McGinnis DE, et al. Reliability and validity of the cocaine selective severity assessment. Addictive behaviors 1998, 23 (4), 449-461.
5. Ahmadi J,Kampman K, Dackis C. Outcome predictors in cocaine dependence treatment trials. Am J Addict 2006, 15 (6), 434-439.
6. Ahmadi J, Kampman K, Dackis C, et al. Cocaine withdrawal symptoms identify “Type b” Cocaine-dependent patients. Am J Addict 2008, 17 (1), 60-64.
7. Ahmadi J, Kampman KM, Oslin DM, et al. Predictors of treatment outcome in outpatient cocaine and alcohol dependence treatment. Am J Addict 2009, 18 (1), 81-86.
8. McGregor C. Amphetamine withdrawal:Nature, time course, and treatment; ph.D. Thesis. Adelaide: University of Adelaide; 2005.
9. McGregor C, Srisurapanont M, Jittiwutikarn J, et al. The nature, time course and severity of methamphetamine withdrawal. Addiction (Abingdon, England) 2005, 100 (9), 1320-1329.
10. McGregor C, Srisurapanont M, Mitchell A, et al. Psychometric evaluation of the amphetamine cessation symptom assessment. J Subst Abuse Treat 2008, 34 (4), 443-449.
11. Hendricks EJ, Greenway FL. Symptoms observed after abrupt phentermine cessation 223-p. Obesity 2009, 17 (Suppl 2), S111.
12. Alexander M, Rothman RB, Baumann MH, et al. Noradrenergic and dopaminergic effects of (+)-amphetamine-like stimulants in the baboon papio anubis. Synapse 2005, 56 (2), 94-99.
13. Wojnicki FHE, Rothman RB, Rice KC, et al. Effects of phentermine on responding maintained under multiple fixed-ratio schedules of food and cocaine presentation in the rhesus monkey. The Journal of pharmacology and experimental therapeutics 1999, 288 (2), 550-560.
14. Rothman RB,Blough BE, Baumann MH. Dual dopamine/serotonin releasers as potential medications for stimulant and alcohol addictions. AAPS Journal 2007, 9 (1), E1-10.
15. Valenta LJ. Letter: Phentermine addiction and thyroxine abuse associated with hypothyroidism. Am J Psychiatry 1975, 132 (5), 569.
16. Ioannides-Demos LL, Proietto J, Tonkin AM, et al. Safety of drug therapies used for weight loss and treatment of obesity. Drug Saf 2006, 29 (4), 277-302.
17. Greenway FL, Caruso MK. Safety of obesity drugs. Expert Opin Drug Saf 2005, 4 (6), 1083-1095.
18. Jain NC,Budd RD, Sneath TC. Frequency of use or abuse of amphetamine-related drugs. The American journal of drug and alcohol abuse 1979, 6 (1), 53-57.
19. Hoffman BF. Diet pill psychosis: Follow-up after 6 years. Canadian Medical Association journal 1983, 129 (10), 1077-1078.
20. Haddock CK, Poston WS, Dill PL, et al. Pharmacotherapy for obesity: A quantitative analysis of four decades of published randomized clinical trials. International journal of obesity and related metabolic disorders 2002, 26 (2), 262-273.
21. Ioannides-Demos LL,Proietto J, McNeil JJ. Pharmacotherapy for obesity. Drugs 2005, 65 (10), 1391-1418.
22. Li Z, Maglione M, Tu W, et al. Meta-analysis: Pharmacologic treatment of obesity. Ann Intern Med 2005, 142 (7), 532-546.
23. Weintraub M. Long-term weight control study: Conclusions. Clin Pharmacol Ther 1992, 51 (5), 642-646.
24. Kim KK, Cho HJ, Kang HC, et al. Effects on weight reduction and safety of short-term phentermine administration in korean obese people. Yonsei Med J 2006, 47 (5), 614-625.
25. McGregor C, Srisurapanont M, Mitchell A, et al. Psychometric evaluation of the amphetamine cessation symptom assessment. J Subst Abuse Treat 2007.
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
By Paula Hendricks - Nutritionist on December 4, 2009
Appetizers for the Holidays – Skip the chips and dip, cookies, and other snacking pitfalls. Make it simple this year with great-tasting and beautiful presentations for your holiday appetizers that are both healthy and full of flavor. Your guests will love them andso will the host when you bring your beautiful dish to your next holiday event. Picturesof these recipes are available in the office.
| Caprese Salad – Such a simple, elegant appetizer! Slice tomatoes, the best tasting you can find in the winter, and cut again in half. In the deli section, buy either fresh cow or buffalo mozzarella. Rinse the cheese and slice into small bite-sized rounds. Layer an appetizer plate alternating with tomatoes and cheese. Cut some fresh basil into small strips and sprinkle over tomatoes. Drizzle some high quality olive oil over the dish, grind some fresh cracked pepper on top, and a sprinkle some kosher or sea salt to finish. | Cucumber Canapes – Top cucumbers with some fresh crabmeat (or imitation crab) that is tossed with a mixture of mayonnaise and Greek-style plain yogurt. Add some salt, pepper and fresh dill weed. Add a little mayonnaise-yogurt swirl to the finished product and sprinkle some capers around plate. Place crab atop fresh endive leaves instead of cucumbers for a different look and taste. Very light and refreshing appetizer. | ||
| Tomato Slices and Chopped Cheese – Slice firm tomatoes into thin rounds; half each round and place on a plate. Cut some hard gouda cheese into tiny bite-size pieces, or other firm cheese of your choice. In separate bowl, mix olive oil, lemon juice and some Italian herb seasoning. Drizzle over the tomato and cheese plate. Top with some fresh chives.
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Shrimp atop Endive – Another elegant presentation. Put bay shrimp in bowl and toss with olive oil, dill weed, minced garlic, lemon juice and a little Dijon mustard. Cut off the end of the endive and discard any brownish leaves. Arrange endive leaves on a platter and add about 1 tablespoon of the shrimp to each leaf. | ||
| Prosciutto and Melon Tasters – Slice honeydew or other melon into small bite-size slivers and put on a plate. Cut prosciutto into manageable bite-size pieces and layer on top of melon. Sprinkle with some fresh shredded parmesan. Delicious.
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Deli Plate – Buy a salami stick (look for a reduced-fat brand), peel off outer layer and cut into thin slices. Further cut the slices into little wedges and place the pieces on a plate. Top with fresh parmesan wedges and add some mini deli pickles to the presentation.
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Happy holidays and happy entertaining!
By Paula Hendricks - Nutritionist on December 3, 2009
Think 30!
Protein intake is your Key to effective weight loss. A daily optimum protein intake of at least 30 grams for breakfast, lunch and dinner allows you to maintain good health while you lose weight. In addition to helping with weight loss, protein helps build and repair body tissues including muscle, major organs and collagen, keeps hair, skin, bones and nails healthy, regulates body processes including digestion and metabolism, and forms hormones, enzymes, and immune system antibodies to help your body function properly. Need any more reasons to think 30?
Use the following list of approximate 30 gram protein choices to meet your Daily Target Protein Intake. Always follow the plan outlined specifically for you.
*Protein grams in food products vary. Always read the nutritional labels and weigh your servings to ensure you are getting the right amount. We recommend purchasing a food scale.
How does the Hendricks family prepare 30 Gram Protein Meals?
Here is a list of some of our weekly favorites:
* Shrimp Cocktail: Chop one celery stick into small bite-sized pieces. Place in small bowl and add 6 oz bay shrimp. Mix together. For the sauce, mix together 1 tsp. mayonnaise, 1 tsp. Greek-style yogurt, 1 tsp. horseradish, 2 T. salsa, and 1 T. low sugar ketchup, and a dash of garlic salt. Add sauce to shrimp and serve chilled. Looks elegant served on butter leaf lettuce cups.
* Vegetable Scramble: In mixing bowl, whip 2 whole eggs, one egg white, a dash of garlic salt and pepper. Add to the eggs 1/2 cup chopped vegetables (zucchini, red peppers, onion) and 1/6 of an avocado. In a non-stick pan over medium heat, melt a tiny bit of butter and pour the egg mixture in. Scramble until eggs are almost set. Add 2 ounces shredded reduced fat cheddar cheese; mix. Place on plate and top with 2 T. salsa if desired.
*Lemony Chicken Cesar Salad: For the marinade, mix the juice of 1/2 of a lemon, 1 T. olive oil, 1 minced garlic, and a dash of salt and pepper. Pour marinade over one 4.5 oz boneless skinless chicken breast and let sit for 10-15 minutes. Grill in a non-stick pan until cooked, about 4 minutes on each side. Cut chicken into strips and lay over a bed of Romaine lettuce. Drizzle 1-2 T. of creamy dressing (see Salad Dressing hand-out) and sprinkle salad with some freshly grated Parmesan cheese. Add a couple anchovies if you like.
* Filet Mignon over Greens: Sprinkle salt and pepper on one petite filet (4.5 ounces) and rub in a little olive oil. In a hot skillet, grill filet on one side for 2 minutes, flip and grill for 2 minutes, and repeat until meat is cooked to your liking. Saute 2 cups of raw spinach in 1 T. olive oil and seasoning of your choice. Place spinach on plate and top with the cooked filet. *
* Omelet with Canadian Bacon: In a mixing bowl, whip two whole eggs, one egg white, 2 ounces chopped Canadian bacon, salt and pepper. In a non-stick pan over medium heat, milt a tiny bit of butter and pour the egg mixture in pan. Cook until almost set. Add 1 ounce shredded reduced fat cheddar cheese. Fold egg in half to form an omelet. Slide omelet onto a plate.
* Tzatziki (Greek Yogurt and Cucumber): In a single serving bowl, put 1 1/3 cup Greek-style thick plain yogurt (ck label to ensure 30 grams). Add 1/2 cup finely chopped English cucumber, 1 small minced garlic clove, 1 tsp. fresh lemon juice, and salt. Mix. Drizzle 1 T. olive oil and sprinkle some dried mint leaves on top of yogurt.
* Deli Meat Roll-Ups: Take approximately 6 oz of your favorite lean deli meat (ck label to ensure 30 grams) and put on a plate. For the sauce, add 1 tsp. mayonnaise, 1 tsp. Greek-style plain yogurt, and 2 tsp. Dijon mustard together and mix together. Spread the sauce on each piece of deli meat and roll up. Add a little crunch and roll some chopped lettuce in each roll.
* Cheesy Lasagna: Mix together 1/2 cup low-fat cottage cheese, 1/2 cup low sugar marinara or spaghetti sauce, and 1/2 cup canned mushrooms (drained). Heat in microwave-safe bowl on medium for about 2 minutes. Add 1/2 cup shredded reduced fat hard cheese (Kraft brand). Mix and serve warm.
By Paula Hendricks - Nutritionist on November 5, 2009
PRODUCTS & SPECIALS
FROM THE DOCTOR
We’re pleased to report that Dr. Hendricks will soon be participating in a cutting edge clinical research project in partnership with staff at the Pennington Biomedical Research Center at Louisiana State University (LSU). The project will investigate circadian blood pressure rhythm (rhythmic biological cycles recurring at 24 hour intervals) in patients newly started on phentermine. Prior research has confirmed that blood pressure varies during the day and night with lowest pressures during early hours of sleep. Normally blood pressure increases in anticipation of arousal, then falls after awakening only to rise again at intervals during the day.
The LSU researchers have shown that some overweight individuals have abnormalities in this rhythm. We will be looking for evidence to support the hypotheses: circadian blood pressure rhythm abnormalities in overweight patients improve with weight loss.
In a prior, still ongoing study, we found no evidence that phentermine directly induces blood pressure changes and that blood pressure falls with weight loss. In the new study, we’ll also be looking for evidence to show that phentermine therapy doesn’t change an individual’s normal circadian blood pressure rhythm and that abnormal rhythms in obese patients improve when weight loss is enhanced with phentermine therapy.
Participating patients will wear an Ambulatory Blood Pressure Monitor which will record blood pressure every 30 minutes during the day and every hour during sleep for one week before starting their weight loss program, for one week early in the program after phentermine is started, and finally for one week after 12 weeks of weight loss. We anticipate a study report will eventually be published in a peer-reviewed medical journal.
This research is another in a series of investigations, dubbed by Dr. Hendricks as “The Phentermine Rehab Project,” intended to publish evidence of the safety of long-term therapy, and to refute long-standing phentermine safety concerns of the FDA and uninformed physicians, hopefully thereby countering governmental restrictions on the uses of weight loss medications.
According to Dr. Hendricks “Phentermine is the safest and most cost effective anti-obesity drug on the market today. It’s a shame its’ use has been marginalized because physicians fear governmental criticism and reprisals for prescribing it.”
FROM THE NUTRITIONIST
– Ingredients: one packet Tex Mex Chili Protein Packet, 10 protein grams of diced Canadian bacon, and 2 T. reduced fat shredded cheddar cheese. Instructions: follow Tex Mex packet directions. Add the bacon and cheese. Mix. Add some chopped fresh cilantro and a dollop of light sour cream.
- Ingredients: one packet Tex Mex Chili Protein Packet & ½ cup cottage cheese. Prepare Tex Mex Chili per directions on the box. Add cottage cheese. Mix and heat. Sprinkle with a little shredded cheese on top.
CALCIUM INTAKE AND BONE HEALTH: by Paula Hendricks, BS, Nutritionist-C
We have updated our calcium recommendations. Please review the following for the latest up-to-date information. I know, it’s a little technical – that is why the new recommendations are delineated first followed by a detailed explanation.
New Recommendations:
As we age, we all want to keep our bones strong, prevent osteoporosis, and reduce the risk of fractures. And if you want healthy bones, all you need is calcium, right? That is what most people believe but it’s not true – calcium supplements alone will help slow down or stop bone loss, which is great, but if your goal is to make them stronger and healthier by increasing bone mineral density, you need more than calcium alone. Eating as we recommend, doing weight bearing exercises, and supplementing with calcium, magnesium, and vitamin D all work synergistically to improve bone health.
Types of Calcium: Most calcium supplements are either calcium carbonate or calcium citrate. Since intestinal absorption of calcium carbonate is dependent on gastric acidity, we recommend taking calcium carbonate after a meal when gastric acidity is high. Calcium citrate isn’t as dependent on stomach acids for absorption and those patients taking medications to reduce acid in the stomach, such as Prilosec or Zantac, should consider taking a calcium citrate supplement. Post-gastric bypass patients should also take calcium citrate.
Calcium Intake: The Recommended Daily Allowance (RDA) for adults is 1000 mg, and after the age of 30 (the end of the bone-growth age), 1200 mg. daily. The maintenance diet we recommend can provide up to 300 mg of daily calcium, without any dairy products. Adding one ounce of low-fat hard cheese can provide 400 mg of calcium, and consuming a variety of protein supplement products sold in our office can add up to 600-800 mg daily.
By adding a 600 mg. calcium supplement in the evening, you should be close to the Recommended Daily Allowance of calcium for the day. If you have any bone health issues, consult with your physician for personal dosage levels appropriate for you.
Calculating Calcium Amounts in Food: To determine how much calcium you are consuming in various products, look for the percentage of calcium on the nutrition label. For calcium, the percentage is based on the recommended % Daily Value intake of 1000 mg. For example, the Cappuccino protein powder nutrition label states that the contents contain 10% of the % Daily Value of calcium, about 100 mg. One Vanilla Ready-To-Drink protein supplement contains 35% of your % Daily Value of calcium, about 350 mg. If you just consumed these two protein supplements every day, you would be adding approximately 450 mg. of calcium to your daily diet.
Vitamin D and Magnesium Intake: Calcium is more readily absorbed in the body if there is an adequate vitamin D blood level. Based on information from the Vitamin D Council, we now recommend that adults take 5,000 I.U. of vitamin D in addition to what is in your multivitamin and what is in your calcium. Children should be on 1,000 I.U. of vitamin D per 25 pounds body weight. These daily doses for adults will improve bone health and provide a multitude of other benefits. In addition to vitamin D, magnesium supplementation of 250 mg daily also aids in the absorption of calcium and incidentally, the combination of calcium and magnesium is a good evening tranquilizer. Who doesn’t need a good night’s rest?
By Paula Hendricks - Nutritionist on November 5, 2009
Chicken Fiesta Soup – Makes 4 Two-Cup Servings
Another Hendricks family favorite! We love the spicy flavor of this low carb hearty soup when the weather turns cool. If you have a large family or want left-overs, I recommend doubling the recipe. For those of you on the VLCD who are keeping your daily carbohydrate count at 20 grams, the carbohydrate count in this soup is approximately 15grams of net carbs per serving.
Ingredients for soup:
Optional toppings:
Instructions:
1. In small non-stick frying pan over medium heat, add 1 tablespoon olive oil; heat. Add the chili powder and mix with oil thoroughly. Continue mixing until chili turns dark, about 2 minutes. Mix in one more tablespoon of olive oil and add the diced onions. Cook for about 2 minutes. Add minced garlic and the tomato sauce. Stir and cook for another minute. Add the diced tomatoes and green chilies. Mix together and turn off heat.
2. In a large soup pot over medium heat, add the diced chicken, hominy and chicken broth. Transfer the tomato mixture into the soup pot and mix contents together.
3. Cook over medium heat for about 15-20 minutes. Add the cumin and oregano. Reduce heat and simmer for another 15-30 minutes. The longer you simmer the soup, the tastier it gets. Add another can of chicken broth, or some water, if you think the soup is too thick.
4. When ready to serve, ladle a serving into a soup bowl and add any of the optional toppings listed above.
Nutritional Value: Each two-cup serving, without toppings, contains approximately 325 calories, 35 grams of protein, 9 grams of fat and 15 grams of net carbohydrates.
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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