Author: Alexis

Medical marijuana has been a hot topic in the medical world for the past few years. A seminar at this year’s Food and Nutrition Conference and Expo entitled “Going green: use of medical cannabis in medical nutrition therapy” discussed the efficacy and use of medical marijuana. Specifically in the second half of the seminar, Zachari Breeding presented the use of cannabis in nutrition related conditions.

He prefaced his talk by discussing the challenges surrounding researching the efficacy of cannabis use. Cannabis is still regarded as a schedule 1 substance, which means it has no currently accepted medical use and has a lack of accepted safety use under medical supervision. The only place to procure research grade cannabis is the University of Mississippi. The university has a very limited amount of space for production, limiting the amount available for research. Not only that, but research into the efficacy of cannabis is rarely funded when compared to research into its detrimental effects. Because of this, there is limited good evidence about the efficacy of cannabis.

However there are still nutrition-related conditions that are qualifying conditions for cannabis use in many states. The most common are cachexia, anorexia, nausea, irritable bowel syndrome, and cirrhosis. With more research, other conditions could also benefit from cannabis use. Two of the main effects of cannabis use researched in nutrition are appetite stimulation and weight gain. In rat models, low dosing of THC was shown to increase both homeostatic and hedonic control of eating. It was also found that cannabis use promoted weight gain, regardless of calorie intake. These uses make cannabis a consideration for treating the elderly who have poor nutrition status. It is also a potential treatment for chemotherapy-related emesis, however most research has found that cannabis use leads to increased food intake because of improved mood instead of increased appetite.

While there are multiple uses for medical marijuana in a nutrition setting, it can’t be prescribed for everyone. There are still risks associated with cannabis as with all drugs. Understanding the risks and benefits is necessary for recommending medical cannabis. Further research is needed on the efficacy of cannabis so that nutrition professionals and their patients can make informed decisions on their best plan of treatment.

Food addiction has become a hot topic in the media, but is food addiction real? In a seminar entitled “Food addiction: fact or fiction?”, doctoral student Carolina Cawthorn questioned if food addiction can be considered a true addiction. She explained that true addiction is when a person compulsively used a substance despite harmful consequences to health, behavior, and relationships.

In regular substance abuse, pleasure is the main motivator for initial drug use. Increased dopamine secretion from drug use becomes a positive reinforcement that drives drug use. At this stage, a person can stop drug use if they want. Prolonged drug use, though, can remodel the brain so it becomes accustomed to the elevated dopamine levels. When the “high” wears off, dopamine levels end up dipping below baseline, causing withdrawal symptoms. The person now takes the drug, not for pleasure, but to avoid distress. The person is now dependent upon the drug and cannot easily stop. Dependency must occur for addiction to occur, however, dependency is not addiction. This seminar tried to discover if not only a person can become dependent on food, but if they can become addicted.

Rat models can be used to simulate human addiction, as they mimic human addiction models and have relatively the same rate of addiction as humans (17% compared to 20%). In an addicted state, as demonstrated by rats self-administered cocaine, they will do more to get the cocaine (bumping their nose to a button upwards off 400 times) and will disregard harmful consequences to get the drug (stepping on a lever and receiving a shock). When repeated with food, only rats who had high-impulsivity and given high-palatability food ate more and did more for the food. Actual analysis of these rat’s brains showed high indication of remodeling. This indicates that rats can become addicted to food, but they have to be susceptible to begin with. Another study showed that rats fed a high-sugar, high-fat diet had significantly less dopamine secretion when switched to a low-fat, low-sugar diet and it stayed down until the high-sugar, high-fat food was reintroduced. However, their dopamine bump from reintroduction was still lower than rats who had only ever eaten the low-sugar, low-fat food getting their regular meal. This indicated a dependency on food. Looking at food-dependency in rat models, it can be assumed that humans can develop similar food dependency.

The Yale food addiction scale (YFAS) is a questionnaire based on the Diagnostic and statistical manual of mental disorders’ codes for substance dependence. It’s used to assess food addiction in humans. It was found there was a 19.9% prevalence of food addiction, the same prevalence as regular substance addiction. But is this true addiction, and not just a dependency? In a German version of the YFAS, the top two symptoms were the “persistent desire or unsuccessful effort to cut down on eating” and “eating anyway – regardless of anything.” This demonstrates a loss of control, but true addiction includes prolonged use regardless of consequences. So how can food addiction be determined? We don’t know. No full conclusions have been made and there is no official diagnosis for food addiction. More research is needed to say if food addiction is on par with drug addiction.

With heart disease being the number one cause of death in America, reducing risk for CVD is a major concern among health professionals. One of the current recommendations is to reduce sodium intake as increased sodium intake, as increased sodium has a positive correlation with blood pressure, and hypertension is a leading risk factor for CVD. Mary (Molly) Cogswell discusses sodium in a seminar titled “sodium intake assessment, monitoring, and applied research”.

The first thing Dr. Cogswell discussed is where to find sodium. We can’t make recommendations if we don’t know where the problem is. First, while a bulk of sodium comes from table salt (NaCl), there are still other dietary sources of sodium, such as baking soda (NaHCO₃). Second, while many recommendations suggest seasoning with less salt, in actuality, that will do very little. Seasoning while cooking and at the table only account for 11% of sodium intake. Pre-processed and restaurant foods account for 71% of sodium intake. This means the biggest way to reduce sodium intake is to change the US food supply. The institute of medicine recommends setting national policies to gradually reduce to sodium used in commercial foods. A similar policy in the UK led to a 42% decrease in ischemic heart disease and a 15% decrease in sodium intake.

The second thing Dr. Cogswell discussed was how to assess and monitor sodium. Accurate measurements are needed in a clinical setting, and especially a research setting, where a small error could be the difference in statistical significance. However, the problem with clinical sodium assessment is, the more accurate a test, the more it costs, which becomes a barrier to many facilities. For example, the 24-hour urinary excretion is the gold standard for sodium assessment. All voided urine over 24 hours is collected and analyzed. This is very labor intensive and time consuming, leading to its high costs. This test still has random measurement error though, since sodium intake and excretion vary day to day. To make it more accurate, the measurement from multiple days would need to be averaged together, which exponentially increases the cost. To make it cheaper, a predicted 24-hour urinary excretion could be conducted. A single sample of urine is taken and used to predict the daily sodium excretion. This is much less accurate, since sodium excretion changes through-out the day, especially at night when the samples are usually taken for convenience. Finding a balance between cost and accuracy is key.

With sodium being such an important factor in reducing CVD risk, it’s necessary to create appropriate recommendations and assessment tools that will help in this endeavor.

In a seminar titled “Snacking among children: essential or excessive?”, Dr. Jennifer Orlet Fischer described some of the problems associated with children’s snack recommendations. Prevailing wisdom from the American Academy of Pediatrics and the United States Department of Agriculture is that snacks are essential to children’s nutrition. There are even federally funded programs to pay for snacking, even though there is not a universal guideline for children’s snacking recommendations. There is currently very little data on young children and snacking. Dr. Fischer presented recently found data over the subject.

The first presented study’s aim was to qualitatively characterize low-income parents’ philosophy of child snacking. What she found seems to be a standard consensus: there is no consensus on what snacking is. Dr. Fischer’s data presented that parents’ idea of what snacking is varied widely. In almost all studies, snacking is self-reported, and so if ‘snacking’ means different things to participants than to researchers, how can accurate data be collected? In the broader scheme of nutrition education, this data insinuates that snacking recommendations cannot be properly followed because they are interpreted differently by different people.

Another interesting facet of the presentation was about the children actually doing the snacking. It was found that, while increasing portion size typically resulted in a child eating more, this was not always the case. A child’s temperament will change how they’re influenced by things such as visual cues. This means a child’s attitude may dictate their food responsiveness, enjoyment of food, satiety responsiveness, and more, all of which affect a child’s risk for obesity. This poses an interesting question. Does snacking cause obesity or does obesity cause snacking? While previous data suggests over-consumption of calories from snacks can lead to obesity, the data Dr. Fischer provided may suggest that obese children are just more susceptible to over-snacking. So we are left wondering, is over-snacking a cause of obesity or a symptom of obesity? Are snacking recommendations needed to help control obesity rates, or are children’s attitudes toward food and snacking more important?

From the seminar presented, we must now consider if universal snacking guidelines for children are even possible. Not only will standardized recommendations be interpreted differently by parents, but a child’s attitude towards snacking will change their snacking behaviors regardless of outside factors. Individual counseling is needed to properly integrate parent’s and children’s attitudes, but snacking needs to be addressed on a nation-wide scale. Can we create a universal guideline that will do no harm regardless of guardian or child attitude? The need is understood, but a practical solution is not easily found.