Have you ever heard of HCG? It is primarily known as the pregnancy hormone, which tested in females can detect an early stage pregnancy. HCG, or human chorionic gonadotropin is generally found in the female uterus, but supplement companies are using it as a weight loss agent. For example, GNC sells an HCG complex which the label claims to "lose up to 30 pounds" with this box. (See image to the right) Ironically, the labeling for these numerous over the counter HCG products states to take with a "very low calorie diet". I have done research in numerous databases trying to find an article consistent with HCG and weight loss and there was only one, from the mid twentieth century, saying weight loss was apparent with a 500kcal diet and HCG supplementation. Obviously with this type of caloric restriction weight loss is inevitable.
It is known that health claims made on labels must be backed up by evidence (possibly a research study) or else the Bureau of Consumer Protection of the FTC will eventually have to pull the product, which is what happened here. The FDA sent out notices to companies producing HCG requiring them to send in a plan of action as to how they are going to correct their mistakes, or fines will be imposed.
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Nine researchers scoured databases and journals for both published records and unpublished documents of ephedrine related toxicity in both English and non-English controlled trials. They separated the cases into athletic performance effect, weight loss (which was broken down into smaller subcategories such as dose-effect and percentage weight lost from week 0) and adverse effects. A specific breakdown after article screening is as follows: 52 adverse events and 20 weight loss. As one looks at weight lost (both ephedra and ephedra plus caffeine) compared to the placebo, there is a consistent increase in weight loss in kilograms of the intervention group. For example, one 20 week study with an equal sample size of 16 persons saw a 1.5kg weight loss with the placebo group and an 8.7kg weight loss with the ephedrine and caffeine group. Noting, as well, that the dosage was 60mg of ephedrine and 600mg of caffeine. This dose was moderate compared to some studies analyzed, such as a 12-week 69 subject design who were given 120mg of ephedrine and 300mg of caffeine. This particular study allowed for a 5.2kg weight loss in the placebo group and a 10.0kg loss in the intervention group. There were no specifics given about exercise and diet during the regiment, but leads us to ask some questions as to what is going on neurologically during this time to allow the placebo group to lose around 12 pounds in a 12 week span by not taking any supplementation. As the researchers looked at exercise-related ephedrine results, the majority of the studies included improved performance in both anaerobic power and increased aerobic time to exhaustion/increased performance in a running scenario. There were 2 sentinel deaths associated with ephedrine along with 3 myocardial infarctions, however this is only occurring 1 in every 1000 persons. There is also no way to distinguish between the events occurring from ephedrine alone or those occurring with caffeine as well, since the majority of supplements taken do indeed include both. With short-term ingestion, there are proven benefits to weight loss and some symptoms of heart palpitations (which are harmless if they are simply premature ventricular contractions and are caused by excitation) and common issues of nausea and jitters.

There have been reported cases of cardiomyopathies with young people who have taken ephedra supplements within close proximity of the dangerous heart condition. The positive correlation between β-adrenergic receptors and ephedra is known to induce myocyte toxicity, causing deterioration of the entire myocardial layer. The first case, of which the subject eventually passed away due to heart-related issues, occurred at the hospital that two of the authors were employed by. A 19-year-old was admitted due to shortness of breath and chest tightness extending out to his left arm. He drank 4-6 cans of beer bi-daily and smoked cigarettes and marijuana a few times a week. His ECG showed a left-bundle branch block which would split up the R wave into two smaller ones due to the time it took for the depolarization to reach the left branch, and it also showed a dilated left ventricle. His cardiac output was lower than normal, at 3.4L/min compared to an average of 4-8. He was put on beta-blockers to block norepinephrine release and an angiotensin-converting enzyme inhibitor to lower blood pressure. He unfortunately died 5 weeks later of a worsening condition of heart failure. This case mentions the combination of caffeine and ephedrine being lethal possibly; caffeine is found in anything labeled "guarana" and the subject's guarana intake was sufficient for inhibiting blood vessel dilation and increasing blood pressure. He was also taking two different supplements with ephedra as the main compound, and in addition to caffeine amplified the sympathetic nervous system and catecholemine release. Another fact that is not mentioned in the journal discussion is that alcoholic cardiomyopathy is incredibly common and considering this young man drank nearly half of a dozen beers every other day could have another cause (or be in conjunction with ephedra use).

The University of Connecticut published a study which analyzed the connection of ephedrine to corrected QT interval time and also systolic blood pressure. The study was conducted because at the time, ephedra was the top-selling dietary supplement (circa 2003) and the majority was used in conjunction with caffeine. At the same time, the association with common use and adverse effects were prominent. The researchers gave a 12mg ephedra/40mg caffeine combination over-the-counter supplement called Metabolife to 15 healthy subjects (most notably no heart issues such as arrhythmias, abnormalities, or palpitations). They were either given the placebo pill on day one and returned 7 days later for the single dose ephedra/caffeine combination pill or vice versa. The QT interval was measured and then corrected using both Bazett's and the Framingham Linear Correction formulas. Corrections must occur due to an increase in heart rate directly affecting the QT time-duration interval, which standardizes them in comparison to a heart rate of 60 beats per minute (1 second R-R interval). Hemodynamic measurements such as stroke volume, velocity index, pre-ejection volume, and diastolic blood pressure were also taken often and the subject was asked at these time points if they had been feeling any adverse effects during the entire trial. The increase in QTc intervals from placebo time trial to dosed time trial were all significant except baseline comparisons. The QTc interval was recorded to be 5.9% higher with the supplementation compared to the placebo group, and the approximate increase was at least 30ms. According to accepted standards, any QTc interval greater than 470ms is considered prolonged, and during this study no subject had a QTc interval greater than 500ms. The hemodynamic effects were noted to increase systolic blood pressure reaching significance and the stroke volume was significant at the .005 level. All of the patients who underwent treatment of the ephedra noted side effects of being jittery or queasy, and one woman was recorded to have tachycardia with palpitations lasting up to 5 hours post-ingestion. Two premature ventricular complexes developed in one patient 5 hours after the ephedra was taken and also went away quickly after. The results of a QTc interval increase such as this one has lead the FDA to pull heart-burn and anti-inflammatory pharmaceuticals cisapride and terfenadine off of the market. The direct relationship between extended QTc intervals is the ventricular arrhythmia torsades de pointes, however in this study it is noted that when the QTc interval was around 490ms the instance of having this issue was only 3.7%.

A case report by the European Society of Cardiology acknowledged a woman who was taking an ephedrine-containing compound who passed away from a "possible relationship" between the two. Left ventricular dilation was present in the autopsy, and the cause of death was said to be cerebral hypoxia due to cardiac arrest. It seems as if there is no clear tie in directly from ephedra to the cause of death, however. Accumulation of the pigment lipofuscin was said to be visible, however this is simply a product of aged cardiac muscle and they are primarily large secondary lysosomes. They are, however, a measure of free radical damage when the atoms attach themselves to a part of the lipid cell membrane, thus ruining it. There was also no evidence of ephedra leading to either the death or hypertrophy of cardiac muscle cells. One issue that ephedra did show correlation with positively, though, is contraction band necrosis and acute ischemia. This occurs when ephedra (a SNS stress stimulant) increase the openings of calcium channels which can cause spasms to the coronary arteries. Due to this, the heart fibers are permanently damaged due to the conformational change of them. It often leads to a prominent decrease in blood flow, which in effect causes the ischemia and possibly death. A marker of myocardial infarction, activation of caspase-3 in conjunction with caspase-9, were both noted to increase in Western blotting analysis in a preserved heart which was of the deceased due to a cardiac cause. On the opposite end of the spectrum, caspase-8 was not found to increase (which is crucial to apoptosis-normally a cascade of events through caspase allows for this to occur). The capsace-3 and capsase-9 activation was not present in the control hearts due to the control hearts of which the subjects died of natural causes. This results in a theory that ephedra toxicity can lead to caspase activation allowing for massive cell death in myofilaments and eventually severely dimish cardiac capacity and efficiency.

The media reports of deaths in the past decade of professional athletes Steve Bechler and Korey Stringer have been the publicity ephedra needed to be pulled off the market in 2004. The autopsy reports have said that ephedra is the culprit of "life-threatening cardiovascular toxicity", when heat stroke was the main cause of death in these two athletes. The research compilation does conclude that ephedra allows for short-term weight loss, but also states that there are toxic levels in recommended dosage. It is said that vasoconstriction, hypertension, and tachycardia are the so-called mechanisms of action in regards to ephedra, with ailments forming such as stroke, cardiac arrhythmias, ventricular tachycardia, and cardiomyopathy. It also states that a study showed a QTc (QT interval with heart rate adjustment) increase to 27ms, which has been reason for removal of other drugs from consumer availability. The most prominent adverse event that happened most often was hypertension, and surprisingly sudden death was a more common occurrence than infarction involving death of cardiac tissue. The article does mention that ephedra magnified previous irregularities, however, which allows for ephedra to not be the prime object responsible for ailments and death of these people. Bitter orange is a substitute for ephedra that has been allowed since 2004, and researchers have noted a halting effect of cytochrome P-450 which is supposed to catalyze the breakdown of medications. This can have dangerous consequences since pharmacists are not responsible for over-the-counter drug, vitamin, and nutrient interactions combined with prescriptions.

A case report by the European Society of Cardiology acknowledged a woman who was taking an ephedrine-containing compound who passed away from a "possible relationship" between the two. Left ventricular dilation was present in the autopsy, and the cause of death was said to be cerebral hypoxia due to cardiac arrest. It seems as if there is no clear tie in directly from ephedra to the cause of death, however. Accumulation of the pigment lipofuscin was said to be visible, however this is simply a product of aged cardiac muscle and they are primarily large secondary lysosomes. They are, however, a measure of free radical damage when the atoms attach themselves to a part of the lipid cell membrane, thus ruining it. There was also no evidence of ephedra leading to either the death or hypertrophy of cardiac muscle cells. One issue that ephedra did show correlation with positively, though, is contraction band necrosis and acute ischemia. This occurs when ephedra (a SNS stress stimulant) increase the openings of calcium channels which can cause spasms to the coronary arteries. Due to this, the heart fibers are permanently damaged due to the conformational change of them. It often leads to a prominent decrease in blood flow, which in effect causes the ischemia and possibly death. A marker of myocardial infarction, activation of caspase-3 in conjunction with caspase-9, were both noted to increase in Western blotting analysis in a preserved heart which was of the deceased due to a cardiac cause. On the opposite end of the spectrum, caspase-8 was not found to increase (which is crucial to apoptosis-normally a cascade of events through caspase allows for this to occur). The capsace-3 and capsase-9 activation was not present in the control hearts due to the control hearts of which the subjects died of natural causes. This results in a theory that ephedra toxicity can lead to caspase activation allowing for massive cell death in myofilaments and eventually severely dimish cardiac capacity and efficiency.

The media reports of deaths in the past decade of professional athletes Steve Bechler and Korey Stringer have been the publicity ephedra needed to be pulled off the market in 2004. The autopsy reports have said that ephedra is the culprit of "life-threatening cardiovascular toxicity", when heat stroke was the main cause of death in these two athletes. The research compilation does conclude that ephedra allows for short-term weight loss, but also states that there are toxic levels in recommended dosage. It is said that vasoconstriction, hypertension, and tachycardia are the so-called mechanisms of action in regards to ephedra, with ailments forming such as stroke, cardiac arrhythmias, ventricular tachycardia, and cardiomyopathy. It also states that a study showed a QTc (QT interval with heart rate adjustment) increase to 27ms, which has been reason for removal of other drugs from consumer availability. The most prominent adverse event that happened most often was hypertension, and surprisingly sudden death was a more common occurrence than infarction involving death of cardiac tissue. The article does mention that ephedra magnified previous irregularities, however, which allows for ephedra to not be the prime object responsible for ailments and death of these people. Bitter orange is a substitute for ephedra that has been allowed since 2004, and researchers have noted a halting effect of cytochrome P-450 which is supposed to catalyze the breakdown of medications. This can have dangerous consequences since pharmacists are not responsible for over-the-counter drug, vitamin, and nutrient interactions combined with prescriptions.

Hypotension is very common during Caesarian section delivery due to spinal anesthesia, which is trying to be combatted by supplementation. Some of the detrimental affects of low blood pressure during this crucial time is nausea, vomiting, decrease in conscious arousal, decreased Q, and diminished blood flow to the fetus. In the field of obstetric anesthesia, there is a wide acceptance of ephedrine as the drug of choice for returning arterial blood pressure levels to normal in cases of maternal hypotension. It is also used as a combative to bradycardia, due to the sympathetic stimulative nature of the drug. In this particular study, ephedra was compared to phenylephrine as to which assisted in raising blood pressure and eliminated bradycardia more, by way of meta-analysis of numerous previous reports. In regards to circulation of the placenta, phenylephrine increased vascular resistance more which is what is wanted in this case-the effect of this being an increase in blood pressure. The umbilical cord pH was also tested, and phenylephrine has been shown to be associated with a lower value than the ephedrine which is a positive for avoiding fetal acidosis (since the closer to zero one is, the closer to the acidic portion of the scale). In conclusion, there is no drug that is a better choice for C-section hypotension since they each have their own benefits and flaws.

Heart rate variability, or HRV, is used to measure how much sympathetic nervous system activity compared to parasympathetic nervous system activity is present. It has been used recently as an indicator of the autonomic nervous system in short time frames, and can be found to parallel certain illnesses. This study interestingly analyzed how ephedra effects the sympathetic nervous system compared to the parasympathetic nervous system. There is a process using ECG leads called heart rate variability (or HRV) to measure the power spectrum of RR intervals in one's heart rate by mode of Hertz. Low frequency is known to be jointly modulated by both vagal and sympathetic nerves (primarily sympathetic, however), where as high frequency is known to be related to respiratory sinus arrhythmia and cardiac vagal activity. Also for reference, %LF is shown by a formula (100*LF/[TP-VLF]) which allows VF and LVF to be included instead of simply just one. Parasympathetic activity is associated with the vagus nerve, so with this action the heart rate is slowed down. The low to high frequency component ratio is also shown to reference sympathovagal balance. Standard protocol of a double-blind study in two 14 day trials where both groups received not only the placebo but the 60mg of ephedrine in the form of ephedra tablets. Results lead researchers to believe that since HF significantly decreased per 120 and 180 minutes post ingestion and LF% significantly increased in all of the time trials besides 90 minutes post. This goes to show that ephedra does predominantly affect the sympathetic nervous system, thus increasing the heart rate and ironically this study (along with every study ever done with ephedra) there have been no adverse side effects to any test subjects.

After reading the entire document report studied in this research article, I am familiar with the exact statistics they are referencing here. The researchers obtained adverse event reports from the FDA and Health and Human Services department of the United States. The cases that were looked at had to be in conjunction with stroke, myocardial infarction, or sudden death in association with ephedra usage in the form of pills or ma huang. The reasons given for usage were primarily bodybuilding, weight loss, energy gain as well as "recreational" (which I am assuming means to feel a high). There were 11 deaths they say were associated with ephedra, and of those 11: 7 autopsies were listed as "normal heart", 3 as atherosclerotic, and 3 as cardiomyopathic. There were ten patients that had myocardial infarctions (heart attack caused by a blockage of the coronary artery), and the odds of 8 of them using ephedra for weight loss is not astounding. The majority of overweight people most likely have some sort of build up of their arteries and high fat diets or else they would not be using a drug for weight loss to begin with. No surprise when 4 of them actually had coronary artery disease which was written in the report of findings. In regards to stroke with ephedra, using my medical background I pulled this apart: ischemic stroke was accounted for in 12 of the 16 patients, and 4 was due to a hemorrhagic stroke. How can ephedra be related to a blockage of blood supply to the brain or a hematoma usually related to blood thinning medications? I feel as if evidence is inconclusive regarding the pull of ephedra off the US market for dietary usage and more research needs to be done.

For thousands of years, the Chinese people have used Ma Huang for an asthma remedy. It was first taken in the form of tea, and since it activates the sympathetic nervous system it actually expands the bronchi to the lungs to allow inflamed vessels to open more easily. In today's society you and I can purchase Ma Huang as Bronkaid, also known as an ephedrine-containing bronchodilating over-the-counter medication. In the early 2000's, the ephedrine kick was on the rise in many supplements from Stacker 2 to Hydroxycut until the FDA banned all sales of ephedra in 2004(minus the forms for respiratory relief) due to "unreasonable risk of injury" while two athletes had recently died from heatstroke, possibly associated with ephedrine usage but never the main and direct cause of death.
Interestingly enough, the have only been two reported cases of death by autopsy fully related to ephedrine. (see image). If you are familiar with over-the-counter ephedrine supplements, one pill is equal to ~25mg of ephedrine which should be taken no more than twice a day. If you look at the picture, it states that both persons took at least 150mg in one dose, 6 times the recommended limit. If we compare ephedrine to alcohol related deaths, according to the Center for Disease Control "there were approximately 79,000 deaths annually attributable to excessive alcohol use" (9). Have you ever heard of something called an EC or ECA stack from your gym-going friends? It is short for ephedrine/caffeine or ephedrine/caffeine/aspirin stack. The appropriate dose is said to be 20mg ephedrine to 200mg of caffeine to 75mg of aspirin, or a 1:10:4 ratio. It is shown in clinical scenarios to promote effective weight loss, as seen from reference 10, a double blind study of obese women taking ephedrine compared to the control of no ephedrine dosage-"weight loss was significantly (P less than 0.05) greater during the ephedrine period (2.41 +/- 0.61 kg) than during the placebo period (0.64 +/- 0.50 kg). None of the patients presented clinically important side-effects." Another study actually researched as many articles regarding ephedrine as they could muster up and put all of the results in an SPSS-based statistical analysis program. Here is what was concluded in approximately 59 or so journalized research articles: "We interpret these data to indicate that the use of the combination of ephedrine and caffeine is associated with a significantly greater (2.2 pound) weight loss per month than is associated with placebo, for up to four months duration."(8)
"To each his own" I say. Since these numbers don't lie and obesity is the number one leading epidemic in America, the FDA should allow supplements to be marketed with a track record of success and stop worrying about the almighty dollar, considering the supplement industry is bringing them so much gosh darn money.

Now remember I said that it is possible to not be starving and yet still losing weight a few articles back? Fiber, healthy fats and complex carbs will make you feel fuller for longer-they take longer to digest than simple sugars. What are some sources of the above-mentioned? Yams and brown rice are phenomenal forms of complex carbs, white potatoes are still a nice starch to add to a post-workout meal without over saturating your blood with a tremendous amount of glucose, and almonds give you a great combo of good-for-you fats and fiber! Insulin is basically a lipolysis inhibitor due to the decreasing of cAMP levels and inactivation of HSL, the rate limiting enzyme of fat breakdown.(11) This leads us to believe that the lesser amount of insulin present after any meal, the better. So what spikes our insulin? Eating those simple sugars that taste great, such as processed crackers and even white rice. The longer the time our insulin is predominantly in the blood, the less time fats are being utilized and higher the concentration of fats being stored. "Free fatty acid (FFA) esterification in fat cells is dependent on...insulin-mediated glucose uptake and glycolysis in the adipocyte"(12). Because of this series of events, it is best to stick with the foods high in fiber and steer clear of those sugars. Proteins are digested and broken down into amino acids, the building blocks of muscle. The twist, of which why some persons advocate a lower carbohydrate and higher fat diet, is because proteins can be converted to glucose not only during a time of low blood sugar or low glycogen content. "The amount of glucose that can be synthesized from a protein depends on its amino acid (AA) composition. This value is about 60 g from 100 g of liver or muscle protein and is based on a knowledge of the total AA content and the proportion of each AA that can be converted to pyruvate." (13) With a possible insulin spike from protein, as we can see, insulin will quickly be released and glucose will diffuse into cells-however with a combination of fats to slow the digestive process, this may have a less profound impact on insulin "spiking" and have a diminished fat immobilization effect.

The focus of this post is a common bark found in some African evergreens (sounds strange, right?) also known as Yohimbe. It has been marketed as a "male enhancement" drug for years, available over the counter as Yohimbe HCl with an average dosage of .2mg/kg of Yohimbe isomers. Surprisingly, it has not been "pushed" by companies as much as it should be, however new research has lead to discoveries that it has a similar effect to the illegal drug Clenbuterol. "How does this work?" you are probably asking yourself. There is such a thing as a sympathetic nervous system-something you may know as the "fight or flight" response in the body to react to a startling situation (and also to exercise). Besides insulin, SNS hormones (also known as catecholamines) are very pertinent regulators of lipolysis due to the adrenoreceptors on which they act upon. Yohimbe just happens to be an a2-adrenoreceptor antagonist, which reverses the dissipating lipolysis effects of the a2-receptor itself. From what is known of this receptor, it is known to inhibit adenylyl cyclase production which in turn creates much less cAMP and eventually a smaller amount of HSL (hormone sensitive lipase) which is ultimately the rate-limiting step in triacylglycerol to free fatty acid/glycerol lipolysis. It is known that the amount of cAMP is a deciding factor in how much lipolysis occurs, however it is not a regulator of how many TAGs are partaking in re-uptake. (insert picture). Research shows that women have higher numbers of a2-receptors in the hips, buttocks, and thigh regions leading scientists to believe this is why women have a higher fat deposit percentage there compared to men, who have higher a2-receptor affinity in the stomach region. To aid in this understanding, it is known that human adipose tissue has the highest density of these a2-adrenoreceptors.
The way these receptors (a2) work is to regulate the release and re-uptake of catecholemines; they are found in the cell membrane of axon terminals and when, let's say, norepinephrine(NE) Is released from the vesicles and activates the a2-receptors which stops the continuation of NE to be released. As previously mentioned, yohimbe is a well known a2-antagonist, which allows NE to linger in the synaptic clefts for longer, diffuse into the bloodstream with a higher content, and not be taken back up by the cells. What exactly does NE do? It is a SNS catecholamine which stimulates b2-receptors, increases heart rate, directly breaks down glucose from glycogen, constricts blood vessels, and increases blood pressure. When research articles are reference much hi be is shown to have a primary lipolytic effect due to SNS activation. "A beta-antagonist was administered to non-obese and obese subjects 60 minutes before yohimbe. This suppressed the b -AR effect of lipolysis induced by increases in NE levels. Plasma NEFA levels decreased, but plasma levels of NE were unchanged" (4); NEFA, or non-esterified fatty acids, are products of lipolysis which are directly related to b2-receptors. Since these receptors were blocked by the dual administration of Yohimbe and b2 antagonists, this goes to shoe that the most prominent effect of Yohimbe is stimulation of the SNS due to the unchanged levels of NE during the study. Ironically people who were tested with taking yohimbe dint report many adverse side effects such as an increase in blood pressure or heart rate, but it is theorized to be because it blocks not only the a2 but also the a1 receptors which are predominant for these types of side effects.
Nutrition, however, can play a part in how this substance can be absorbed and may alter it's role in effective lipolysis. Pancreatic beta cells also have a2-adrenoreceptors located in the cell membrane which are also affected by yohimbe's antagonistic effects. Since beta cells produce insulin, when glucose is present Yohimbe actually increases insulin production and in turn shuts down lipid mobilization. Because of this, it is recommended that one takes the herbal supplement on an empty stomach with a diet in accordance with high protein and fat levels, which will attempt to lower insulin levels separately.

Where can you find Yohimbe? At your local health food store!

As some of you may have heard from your RD or internal medicine physician, the Atkin's Diet is a "bunch of malarky" (in the words of my grandma). What exactly is the Atkin's approach to fat loss, what is so terrible about it, and are there any alternatives? First and foremost, it is a low-carbohydrate approach to weight loss and according to professionals your cholesterol will skyrocket and your fat levels will be through the roof. A typical Atkin's plan puts one on an induction phase of strictly proteins and cheeses, and then a maintenance phase of other foods without direct carbohydrate sources. What exactly is a carb? Anything that is made up of glucose, grain, and sometimes fiber. Romaine lettuce is surprisingly a carb, carrots are carbs, and even milk is a carb! Now has your doctor ever told you what cholesterol is? It is a waxy substance made up of lipoproteins that can stick to the walls of our arteries causing a build up of plaque. What Dr. Atkins fails to tell us is that exercise is also crucial to maintaining a great physique-which can also lower our bad cholesterol and increase our HDL, or good cholesterol, levels.

A study done in 2005 showed that following a long term low carbohydrate diet actually significantly decreased LDL levels, blood triglyceride levels, blood glucose levels, and significantly increased HDL levels along with significant weight loss. The foods the researchers relied on during the study were proteins ranging from tuna and sausage to chicken and full fat eggs/cheeses. There are various ways to modify a ketogenic diet to limit the amount of fats present, but if you take note that the breakdown of proteins is ~40% glucose, higher fats are needed to indeed stay in a state of ketosis. Each meal of 6 per day should include a protein and a fat, preferably one lower in saturated fats. According to a website, www.AtkinsExposed.org, "The warnings from medical authorities continue to this day. "People need to wake up to the reality," former U.S. Surgeon General C. Everett Koop writes, that the Atkins Diet is "unhealthy and can be dangerous". However there is no detailed information regarding this unhealthy and dangerous claim, especially after looking at the above mentioned study.

I am not necessarily an advocate of Atkins himself,but rather ketogenic diets as an effective weight loss method. Atkins fails to suggest monitoring fats and combining certain ones, however one of the frontrunners of ketogenic dieting in the sport of bodybuilding touches on this well (Dave Palumbo). He makes it known to, first and foremost, cut the cheese. Cheese is a source of protein, yes, but it is so high in bad fats and calories per ounce. Talk about calorie dense! Per ONE ounce of normal fat cheese(approximately the size of 3 stacked dice) it would take the average 150lb person 15 minutes of running to burn it off! At 9.3g of fat, 5.9 of it saturated, and 7g of protein.per ounce, one could substitute 4 egg whites and a sugar free jello for 1/3 less calories and a satiating meal, along with 17g of protein instead of 7! A handful of almonds can also be added for a healthy addition, with plenty of fiber and polyunsaturated fats.
Are you scared of your blood becoming acidic since your doctor said this is such a dangerous part of Ketosis? Well if you have diabetes, he is correct. You will not be producing insulin, allowing your blood to become thick and viscous due to a build up of both glucose and because of the low carbs, ketones. Normal people have insulin available to compensate for this mechanism, which is normally not mentioned. Fats become broken down into ketone bodies to provide energy and also some proteins do as well-however there is some glucose formed from gluconeogenesis of proteins available despite what you may have heard otherwise.

Personal Trainer? Nutritionist? DIetician? Bodybuilder? Where Should I Go?

In my honest and educated opinion, the best place to find information on subtopics such as competitive fitness nutrition and supplementation are both google scholar and informed professionals. If your goals are beginning to lose weight and lower your blood pressure, an RD(registered dietician) would most definitely be the way to go. However, if you are looking to tone your physique for a more muscular appearance or for a contest, I would recommend asking someone with a degree in either exercise physiology or nutrition with a background in the other, biochemistry, and personal experience with this type of enhancement. There is no way one who has never done a contest diet like a bodybuilder can give you information on how to do it, unless he has a proven track record of success. Make sure that you ask to see credentials first since there is no personal training accreditation organization (anyone can call themselves a personal trainer) and also ask to see previous clients' results or have the opportunity to speak with them. There are also other resources in this field: many articles may not be from a journal or research article, but muscular development and rxmuscle for example. They are usually medical doctors or PhD's with a focus on bodybuilding and supplementation and will always supplement their articles with numerous published journal citations to cross reference their analysis. If you are interested in one section of an article more than another, you can go to the superscripted number by that section in the article and scroll down to references to find the appropriate matching number which indicates the source.

If you've ever seen a self-proclaimed fitness guru in person, male or female, it can be a little intimidating. It may be the impeccable tan or cuts separating their shoulders from their arm muscles, but whatever the case may be as long as you're not seeing bones these people probably eat more calories than you do. But what, exactly, is their choice of fuel? Not Starbucks or Bisquick, I can say with confidence. But if not a light mocha sans whipped cream and pancakes made with skim milk, there are better calorie-sparing options. Calories in versus calories out is the fitness enthusiast's quadratic equation, and programs like MyFitnessPal (available on iPhones and Android devices) are like scientific calculators for engineers. If one's basal metabolic rate is 1700kcal per day; in other words without exercise, daily duties of the ever-loved kitchen floor mopping (or in my case,swiffer-ing), or the thermic effect food digestion emits the amount of energy one's body uses for fuel, we can get a healthy 1500 calories in our bodies with 100% of daily vitamins and minerals. Without doing hours of cardio, we will still feel satiated and be losing around one pound a week.

If you decide to train for a 5k or throw some weights around, this can easily be upped to 1.5-2 pounds a week, which is still considered healthy. Splitting meals into 6 small portioned groupings of appropriate macronutrients can boost positives of body composition, which is backed up by ages old research. When we compare 3 large meal feedings to "nibbling", or smaller meals throughout the day,the results of a study were as follows: "increase in body fat, decreased body protein, altered thyroid activity, and an increase in diabetes mellitus"(14). Not all of the mechanisms of action are known fully, but we do know that through more frequent thermogenesis (due to food digestion) and the possibility of breaking down proteins due to the lack of glucose available-if meals are eaten at 6am for breakfast, 1pm for lunch, and 6pm for dinner that is 6 hours of glucose breakdown depending on what type of activity one does. Eating more often also makes one more full, especially with the addition of a healthy fat to a meal-again going back to fats taking longer to digest, you literally will be breaking down food for a longer time period and it will be sitting in the stomach for a larger duration compared to, let's say, just a piece of toast with jam alone.

A normal diet plan for someone looking to tone up and show off the muscle they built is as follows, along with a multivitamin:
Meal 1: 3 egg whites, 1 whole egg, a bowl of Kashi protein plus cereal with skim milk
Meal 2: protein oatmeal-1 scoop of a whey isolate or soy(preferentially for women) mixed into a low sugar oatmeal, like Quaker Weight Control
Meal 3: large salad with a mixture of spinach & romaine lettuce, tomatoes, broccoli, carrot, cucumber, sunflower seeds, grilled chicken, mixed with olive oil and balsamic vinegar, 1/2 cup of brown rice with I Can't Believe It's Not Butter Spray and sriracha sauce
Meal 4: protein pudding-1 scoop of whey mixed with 2Tbsp peanut butter, 1tsp canola oil, 1egg white, dash of water microwaved for 1min; sugar free jam with a piece of whole grain Ezekiel bread
Meal 5: salmon with capers, asparagus with walnuts, and a yam
Meal 6(before bed): casein protein shake or 2Tbsp peanut butter with fat free cottage cheese

14. Cohn, Clarence, and Dorothy Joseph. "Effects on Metabolism Produced by the Rate of Ingestion of the Diet." American Journal of Clinical Nutrition 8 (1960): 682-90. AJCN. Web. 6 Sept. 2011. http://www.ajcn.org/content/8/5/682.full.pdf