Cupping therapy has been used for over 2000-3000 years, with it’s beginnings in Chinese medicine. There a few variations of this technique (fire cupping, wet cupping, dry cupping, massage cupping) that uses suction within glass jars in order to relieve a variety of bodily ailments.
Recently, I was able to have this technique performed on my back for muscle tension and back pain – in this case, fire cupping was used to create a vacuum within the jars. I wasn’t aware of what I was in for when I told my friend she could perform cupping therapy on me. While I laid on my stomach, she lit cotton balls soaked in alcohol on fire, placed them inside the cups to create a vacuum and then suctioned them to my back. The experience was extremely painful – she left some jars in place on my upper back while she moved others around on my lower back as a massage technique. She left the stationary ones on for about 20 minutes while using the ones on lower back as a massage procedure. While this was happening I was questioning what I had gotten myself into and wondering if I made a bad decision! However, after the procedure was finishing and she removed the cups from my back, I felt amazing. There was no pain after the procedure even though my back looked like it was attacked by a large octopus. The tension in my muscles was released and my lower back pain was completely gone. For me, this technique relieved my muscle pain better than deep tissue massage therapy.
Not until after the therapy did I actually look more into cupping. I was amazed to find many articles about the benefits of the procedure and the ailments that can be treated with cupping (cough, herpes, Bells Palsy, muscle pain, acne, and herniated disks).
Personally, I would rather treat a condition using holistic methods as opposed to surgery or medication. If this technique is still in use from 3000 years ago and still effective, I would recommend others to try it at least once or twice before considering other more invasive options. The pain is only temporary and worth it for the benefits gained from the therapy.
1. An updated review of the efficacy of cupping therapy. Huijuan Cao, Xun Li, and Jianping Liu. PLoS One 2012.
Well here it is, almost winter again with our days getting dark around 4:30pm (before most of us even leave work). Sunlight is extremely important for setting our daily rhythms such as sleep, eating, productivity, and energy – by suppressing the neurotransmitter/hormone melatonin (a chemical that causes sleepiness). Melatonin is secreted in the brain by the pineal gland. Melatonin levels increase with darkness and decrease in the morning with sunlight. For that reason, every year at this time I find myself tired all the time and sleeping a lot. Not only that, but I feel like I have less motivation to actually go out and be social. My office lacks windows so I don’t even get to absorb what little daylight there is during work hours. So, I feel like that big guy in the picture, a hibernating bear
I’ve never been officially diagnosed with seasonal affective disorder (SAD – how appropriate), but I have all the symptoms. Symptoms of SAD include hypersomnia (excessive sleeping), daytime sleepiness, increased negative mood in fall and winter months, lack of energy, and 80% of cases are in women during childbearing years.
There are a few options available for improvement of SAD symptoms, but none of them were shown to completely abolish the negative impacts. The first is light therapy by using a light box although some prefer tanning (which I do not recommend!) even though reports of this technique has conflicting results. The time of day the person is exposed to bright light seems to have significant impact. It is helpful to try to get outside a few times a day to take a walk just for some natural sunlight exposure (probably the most effective therapy in SAD treatment). A second option is exercise (in my opinion probably the second most helpful therapy) – multiple studies have shown the importance of exercise for improved mood and energy. The third option is anti-depressant medications such as monoamine oxidase inhibitors, norepinephrine/dopamine reuptake inhibitors and selective serotonin reuptake inhibitors. However, finding the right medication and dose could take weeks to months (it could be spring by that time!). I’ve also written about food and mood before, so eating more healthy foods during the winter months could lower negative impacts of SAD – this includes reducing the amount of sugary starchy carb loaded food (put down that Christmas cookie!) so that insulin levels don’t spike and drop quickly. Lastly, from personal experience I have found that just getting out and socializing (even when you don’t feel like it) increases mood significantly – if you can incorporate it with activity it is even better (think about joining a sports league with some friends).
If you can combine all of the above suggested treatments I think that is the best option for minimizing SAD symptoms, increasing mood, and increasing energy levels. I would love to hear some comments from others about their methods for treating SAD.
I met a woman over the weekend who told me that she had been diagnosed with early onset Parkinson’s disease (PD) after she learned that I studied the effects of pesticides on brain development. I felt sympathetic towards her because she is only 39 years old and is on several medications and recently went through surgery for deep brain stimulation (DBS) to try to minimize the effects of the disorder. She told me that before people are aware she has PD she had been called “mumbles” because she has a hard time enunciating her words. She also told me the meds that she is on for the disorder cause her to act differently than she used to. Despite all she has been through, she remains positive and upbeat about her situation which really impressed me.
Parkinson’s disease is a disorder in which areas of the brain involved in dopamine release start to degenerate. Dopamine is a neurotransmitter needed for motor control. Over time, this loss causes movement problems, tremors, and difficulty walking and talking. While there are medications given to patients with this disorder, they can only treat it and slow down its progress. Deep brain stimulation is an effective treatment for PD, yet is highly invasive with a pacemaker inserted into the brain so the patient can use a remote to inactivate or stimulate areas of the brain depending on the symptoms of the patient.
Currently, the causes of Parkinson’s disease are unknown, albeit much attention is on the role of environmental toxicants. Roughly 5% of PD cases are solely from genetic mutations. Even though there is no specific cause of PD, individuals that are ‘genetically predisposed’ are at a higher risk for the disorder, especially in conjuction with environmental toxicant exposure. Earlier studies reported that certain pesticides disrupt locomotor activity and alter dopaminergic neurons and dopamine release from those neurons. Just this month, scientists from University of California San Diego published a study indicating that the herbicide Paraquat and the fungicide Maneb affect the growth of new neurons in the adult brain and the expression of genes involved in the formation of new neurons (using mice). Both Paraquat and Maneb have been found in a large number of non-organic foods. Maneb was banned since 2010, but was in use since the mid-1900s. Paraquat is one of the most used pesticides, since 1955, even though it is extremely toxic. Farm workers exposed to these pesticides have an extremely high risk of getting Parkinson’s disease.
I’ve written about pesticides before, but it doesn’t hurt to reiterate to make you aware of what you are putting in your body. Even though you probably aren’t a farmer exposed to high levels of pesticides, studies show that eating organic foods drastically lowers the levels of pesticide metabolites in the body. We all know that eating organic is more expensive, but it might be worth giving up some other non essentials to invest in our health. With the abundance of research on the harmful effects of pesticides, we can’t ignore the facts that they are poisoning our bodies and our environment. At the very least, take a look at the “ The dirty dozen ” foods with the highest amount of pesticide residues and try to incorporate those into your diet. I think it’s time that being pro-organic shouldn’t be the minority anymore!
Desplats, PA. et al. Combined exposure to Maneb and Paraquat alters transcriptional regulation of neurogenesis-related genes in mice models of Parkinson’s disease. Mol Neurodegener. Sep 2012 28;7(1):49.
Arkury TA et al. “Pesticide Urinary Metabolite Levels of Children in Eastern North Carolina Farmworker Households.” Environ Health Perspect Aug 2007;115(8).
Well we sure have heard a lot about the zombie apocalypse lately, haven’t we? It seems like every month there is a new report about someone getting high on bath salts or synthetic marijuana that ends up hallucinating and becoming cannibalistic. I even read a report about a man who ate his own dog after getting high on synthetic marijuana (!!?!?!?). It makes me wonder why, after all of these reports, are people still trying to get high from these drugs?
The ease of finding these drugs are one of the appeals of using them. While the government has become more strict in the sale of these drugs, they can still be found easily in different forms on the internet, in head shops, or convenience stores. Temporary restrictions were recently implemented on some forms of both drugs already, but since they are synthetically made, many new forms are popping up, making them hard to restrict in sales and use.
While bath salts and synthetic marijuana have different mechanisms of action on the brain, they elicit similar responses in people who ingest, inhale, or smoke them. Synthetic marijuana (or also known as “spice” or “incense”) binds to the same receptors in the brain that natural marijuana does. However, in the synthetic form, they are full agonists of the receptor – meaning they have a way more potent effect than natural marijuana does and they can have longer lasting effects – there is no ceiling of toxic ingestion. Bath salts work by increasing levels of monoamines in the spaces between the neurons – especially dopamine. This means that dopamine sticks around longer and binds to more receptors on adjacent neurons. In normal levels, dopamine helps regulate sleep, wake, reward, mood, attention, memory, learning, and sexual satisfaction. However, high levels of dopamine can create all sorts of crazy, not to mention harmful, side effects.
Patients who were administered to the ER under the influence of bath salts and synthetic marijuana experience many of the same symptoms: Paranoia, seizures, rapid heart rate, increase blood pressure, delirium, agitation, hallucinations, delusions, and psychosis. However, the most disturbing effects of these drugs are the emergence of zombie like behaviors including cannibalism, suicidal ideation, and extreme violence towards people and animals. Because of the recent increase in these drugs, many long-term side effects are not known and have not been studied (and potential addictive qualities of these drugs are hard to determine).
This blog serves as a warning to anyone who is using these drugs or knows of anyone using them. Please, think twice (or more!) if you are interested in using them.
Jerry, J., Collins, G., Streem, D. 2012. Synthetic legal intoxicating drugs: The emerging ‘incense’ and ‘bath salt’ phenomenon. Cleveland Clinic Journal of Medicine. 79:4
Penders, T.M. 2012. How to recognize a patient who’s high on “bath salts”. The Journal of Family Practice. 61:4
I didn’t used to think so either…
This is what I would look forward to every morning! This is what made me want to get out of my warm cozy bed. I love the smell of coffee, the taste of coffee, and that little kick it gives me when I wake up (which is becoming more needed the older I get). However, I decided a few days ago that I needed to give up my daily caffeine addiction.
So, last week I was feeling awful… I mean I literally didn’t want to move… it was tough getting out of bed, I had headaches, and after work all I wanted to do was nap and not get off the couch. I made it to the gym but barely had a good work out – and afterwards I was shaking, weak, and light-headed. Of course my remedy for this was to have even more coffee – in addition to the 4 or 5 cups I was having every morning. I wasn’t realizing this was making my situation worse. The last straw was Sunday night, when I had the brilliant idea of drinking the iced coffee I had left in the refrigerator earlier that morning. After I drank it, I had one of the worst headaches ever – and then I asked myself “what would happen if I just didn’t have coffee tomorrow?”
The next day, not having any coffee, I felt better than I had in weeks! I had more energy and felt more focused and my muscles didn’t feel weak like they had the past few weeks. So I decided to do some searching on PubMed for any studies linking coffee and fatigue. I already knew the two were linked because of a study I performed in my own lab. Super high doses of caffeine actually have the opposite effect than low doses. In the zebrafish that I study, high caffeine caused the larvae to swim at much slower speeds than the ones treated with low doses of caffeine.
But I also found a very interesting case study that completely described the symptoms I was having. In a report in Clinical medicine insights: case reports from 2007, there was a woman admitted to the hospital that developed rapid muscle weakness and general fatigue. After several blood tests, the doctors diagnosed her with hypokalemia (which is a severe loss of potassium in the body). Apparently, she was drinking large amounts of coffee daily which subsequently leached the potassium out of her body because coffee is a diuretic.
Potassium is essential for proper nerve firing and normal muscle cell functions. When blood potassium levels become too low muscles become fatigued (with spasms), there is presentation of abnormal heart rhythms and palpitations, and paralysis can occur with severely low levels of potassium. After reading this article, I decided to keep going on my no coffee (or other caffeinated products) experiment. Going off caffeine completely isn’t the most pleasant experience. I was definitely having withdrawal symptoms (headaches, tiredness), but overall I felt 100x better than I did last week. I actually had two great workouts finally and didn’t feel like I was going to pass out when I finished. I may eventually add coffee back into my diet, but for now I am feeling great without it.
While this is a documented clinical case report, there still are many other factors that could have contributed to the patient’s symptoms. While coffee-induced hypokalemia exists, it isn’t widely reported. This is a great reminder that even the good things in life need to be appreciated in moderation.
2) Richendrfer H, Pelkowski SD, Colwill RM, Creton R. On the edge: pharmacological evidence for anxiety-related behavior in zebrafish larvae. Behav Brain Res. 2012 Mar 1;228(1):99-106. Epub 2011 Dec 6.
Are you an extrovert or an introvert? Personality types are often lumped into one of these categories. Frequent social engagement and novelty-seeking behavior are characteristic of extroverts, whereas introverts prefer to be alone and engage in familiar activities. The differences in brain chemistry that cause these personality traits arise from both ‘nurture’ or individual experiences, and ‘nature’ or genetic predisposition. But which one is more important? This is a classic theme in neuroscience that I will not fully explore here; but new evidence from honey bees scores another point for team nature.
A recent article1 published in Science by Liang et al. investigates the molecular basis for novelty-seeking behavior in the honey bee, Apis mellifera. The authors seek to understand how individual differences in gene expression lead to behavioral variation. They explain that 5-25% of bees within a population continually seek new food sources, even when there is no food shortage. Other individuals stick to the hive and only venture to new sites after the pioneers or “scouts” have told them the way. But how do bees communicate?
Unlike ants or termites, bees can’t leave a trail of pheromones for others to follow because volatile chemicals like pheromones dissipate in the air. Instead honey bees have come up with a creative mapping strategy. They encode the location of newly found food sources within a complicated series of movements called the “waggle dance.” First discovered by Karl von Frisch in 1965, the waggle dance is only performed by scouts2.
So what determines if a bee has what it takes to be a scout? As it turns out, dance moves aren’t the only criteria.
Liang and colleagues collected honey bees that consistently displayed scouting behavior and analyzed gene expression in the brain. Several differences in neurotransmitter signaling were found between scout bees and non-scouts. For example, genes that encode receptors for glutamate, a major excitatory neurotransmitter, had increased expression levels in scouts. A direct relationship between glutamate signaling and novelty-seeking was demonstrated when bees that were given MSG (mono-sodium glutamate) showed increased scouting behavior after administration. Differential expression of DopR1, a gene encoding a subset of dopamine receptors, was also found. Blocking dopamine signaling resulted in an overall 44% decrease in scouting behavior.
The authors point out that both glutamate and dopamine are known to be involved in novelty-seeking behaviors among many vertebrates. Interestingly, DopR1 is known to be involved in drug-seeking behavior in humans3. Although the brain circuits involved in this behavioral dichotomy have not yet been sorted out, it is clear that a similar pattern of gene expression is involved in what I like to call adventurousness. Perhaps a closer analysis of the relationship between genetics and adventurous behavior in other animal models will provide a basis for identifying genetic predisposition to drug addiction or even thrill-seeking in humans.
Written By Alyssa R. Wheeler
1. Liang ZS, Nguyen T, Mattila HR, Rodriguez-Zas SL, Seeley TD, Robinson GE. Molecular determinants of scouting behavior in honey bees. Science. 2012 Mar 9;335(6073):1225-8. PubMed PMID: 22403390.
2. von Frisch K. [The "language" of bees and its utilization in agriculture. 1946]. Experientia. 1994 Apr 15;50(4):406-13. German. PubMed PMID: 8174688.
3. Le Foll B, Gallo A, Le Strat Y, Lu L, Gorwood P. Genetics of dopamine receptors and drug addiction: a comprehensive review. Behav Pharmacol. 2009 Feb;20(1):1-17. Review. PubMed PMID: 19179847.
So imagine my delight in coming across not just one, but two scientific articles about zombies. Both of these papers investigate the real-life phenomenon of zombies in Haiti, where the idea of the zombie originated. The traditional explanation for zombies is sorcery. The Vodun religion (also known as Voodoo) makes a distinction between different elements of a human being. There is the corps cadavre (the physical body), the gwoban anj (the animating principle), and the ti-bon anj (agency, awareness, and memory).
Haitian zombies aren’t really undead. They are the result of a sorcerer taking the ti-bon anj of the victim, leaving a passive and easily-controlled body. These zombies are then believed to be used as free labor on Haitian plantations. Haitian zombies are easily identified by the community. They cannot lift up their heads, have an empty staring expression, and have limited and repetitive speech.
Poisoning was one theory to account for zombification, and in the early 1980s, anthropologist and ethnobotanist Wade Davis traveled to Haiti to investigate. He interviewed Vodun sorcerers and obtained samples of a white powder called coupe poudre that they used to zombify their victims. Analysis of the samples revealed a number of pharmaceutically active ingredients, including cane toad (Bufo marinus) toxins, an irritant produced by a tree frog (Osteopilus dominicensis), and tetrodotoxin, a neurotoxin produced by puffer fish and other marine animals.
Davis hypothesized that the irritant causes small wounds on the skin of the victim, through which the tetrodotoxin enters the bloodstream. The potent toxin can kill by paralysis, but sub-lethal doses result in a significant reduction in heart rate and metabolic activity. Victims, completely paralyzed but fully conscious, are pronounced dead and buried. After a few days, the sorcerer returns and claims the body. The victim is kept enslaved in a permanent state of delirium and disorientation with more drugs, likely containing atropine and scopolamine, toxins with hallucinogenic properties derived from the plants Datura stramonium and Datura metel. In Haiti, both of these plants are known as the “zombie cucumber.”
Recently, scientists publishing in the journal Evidence-Based Complementary and Alternative Medicine revisited Davis’ zombie potions, analyzing the chemical, biological, and pharmacological components of the powders to determine if tetrodotoxin really is the most important ingredient. They came to the same conclusion as Davis and identified four species of puffer fish as the reason behind the poison’s efficacy.
Pufferfish tetrodotoxin blocks sodium channels and prevents neurons from firing. People who ingest the toxin and don’t die within the first 24 hours typically survive, although they often fall into a coma-like state for several days. During this time, they may appear to be dead; reduced metabolic activity decreases the body’s need for oxygen, and the diaphragm muscles may be partially paralyzed, making breathing difficult to detect.
Tetrodotoxin is certainly a potent neurotoxin, but even Davis emphasized that the zombie powder is just one requirement for zombification. Equally important are cultural expectations involving the power of Vodun sorcerers and the effects of the powder, which are learned and ingrained in many parts of Haitian society.
In 1997, the medical journal The Lancet published a medical investigation into three “returned zombies” —individuals whom family members identified as having died and then returned, sometimes decades later, as zombies.
Doctors performed full medical exams on the zombies, including EEG and CT brain scans. The first subject had no neurological damage but was diagnosed with catatonic schizophrenia. The second subject did suffer from brain damage, probably due to lack of oxygen and untreated epilepsy. The last subject was diagnosed with a developmental learning disability, possibly fetal alcohol syndrome.
The most interesting finding came from DNA and fingerprinting tests that revealed that two of the zombies were cases of mistaken identity. They were not the dead relatives that the families identified.
It is unlikely that there is a single explanation for all cases of zombification. Poisoning by tetrodotoxin can cause symptoms typical of Haitian zombies, and it has been shown to be an ingredient in so-called “zombie powder.” But this study suggests a simpler answer: many zombie cases are mistaken identification of wandering mentally ill or neurologically injured people by grieving relatives, primed by their culture to accept the notion of zombies. The authors write that “People with a chronic schizophrenic illness, brain damage, or learning disability are not uncommonly met with wandering in Haiti, and they would be particularly likely to be identified as lacking volition and memory,” instantly recognized zombie characteristics.
Is the mystery of zombification solved? Sort of. It may be that there are as many types of real-life zombies as there are cinematic ones.
Music has incredible power over the human psyche, and in particular over memory. While we’ve now begun to uncover the underlying scientific principles linking music to memory, the phenomenon is something that songwriters and lyricists have known for years. Cole Porter’s classic “Begin the Beguine” explicitly addresses the strength of this connection; throughout the song, the singer recalls that, when the band starts to play music he associates with a former lover,
it brings back the sound
of music so tender
it brings back a night
of tropical splendor
it brings back a memory of green
and that, every time the tune plays, he can’t help but re-live the precious moments spent with the lady he’s lost—even though he tries his best to forget her.
The experience sounds familiar to many of us. When I hear old Clapton ballads, for example, I recall a very particular dance, memories refreshed like a series of old photographs, every detail perfectly catalogued, right down to the curls in my hair and the color of his vest (it was blue). When I go for a run on a warm, blue-skied afternoon and “Sweet Child O’ Mine” pops up on my workout playlist, the song calls to mind every outdoor barbecue, every trip to the beach, every open-windowed drive on hot pavement, every sunny day when that song might have played, and I inevitably find myself grinning, glorying in the beautiful weather and the sound of summer. How can music do this for us? How is it that even a few seconds of a tune, an echo on the radio, can evoke such powerful memories?
The study of music and memory is still relatively young, but what we know thus far is that part of the strength of music as a stimulus or memory trigger seems to be linked to emotion. In the memory field, strong emotions are generally thought to enhance memory formation, as well as memory recall. This concept makes intuitive sense; isn’t it easier to recall exactly how you felt when you had your first kiss, and what you smelled, and saw, and heard, than it is to recall how you felt when you ate that (presumably emotionally neutral) ham sandwich the other day? The effect of emotion on memory formation makes evolutionary sense, too: intense emotional arousal (e.g., fear) would strengthen memories concerning, say, a close encounter with a predator—an important experience for our ancestors to remember (and hopefully avoid in the future)!
This sort of enhancement is mediated in part by a brain structure known as the amygdala. The amygdala makes bi-directional connections to many other parts of the brain, allowing it to communicate with (among other regions) the hippocampus (responsible for memory formation), the pre-frontal cortex (associated with mood and other complex processes) and the hypothalamic-pituitary-adrenal axis (a network that can stimulate the production of hormones that may modulate memory formation and consolidation). About ten years ago, a study found that some of these same brain regions can be activated by music! Specifically, amygdala activation was associated with music that produced the intense feeling of “chills.” Various studies since that time have implicated other components of the limbic (emotion) circuitry in the brain’s response to music, strengthening the apparent connection between what we hear and what we feel. Music has also been shown to enhance our emotional responses to visual stimuli. Imagine Mufasa’s death without the music. Imagine chase scenes in the Bourne movies without the frenzied strings. Considerably less memorable, right?
What’s especially interesting is that music has been linked to the activation of other brain structures, including the nucleus accumbens. Remember the nucleus accumbens? It’s associated with feelings of pleasure, fun, and reward—which, among other reasons, make this brain region integral to addiction behaviors. Still, the activation of reward circuitry by music has a number of interesting implications. Among the most clinically salient, however, are these:
Could we use music to help address mood disorders, or anxiety disorders?
Could we use music to modulate our perception of emotional experiences?
Given the link between music and memory—could we use music to promote memory formation and recall in patients with memory disorders (like Alzheimer’s disease)?
And in fact, these questions are all topics of current and intense research within the field of music perception.
So next time you turn on the radio, think about the songs you hear, and what they might mean to you and to your personal history. Maybe you’ll hear an old love song as you’re driving home from work today; maybe it makes you want to cry. Or laugh. Or feel and remember any of a thousand different things, thrusting you headlong into any of a thousand different moments, each distinct and based upon your own experience—consider it an autobiography of a sort, your life and mine, called to mind, refreshed, re-lived in a series of chords.
Did you ever say to yourself “I will just have a small piece of ________ (cheesecake, ice cream, cake… fill in the blank!)” and end up eating way more than you wanted to? Did you ever notice that when you “fall off the wagon” of eating healthy, it’s harder to get back to eating healthy than it is to give into junk food?
A recent review article in the journal Frontiers in Neuroendocrinology by Johan Alsio, Ph.D. and others illustrates how much our bodies are made for holding onto fat by way of brain changes, variations in hormone levels, and molecular adaptations during overeating.
In our society, we tend to eat not only from hunger, but from food cravings even at the risk of gaining weight, developing diabetes, and increasing our cholesterol levels – if left unchecked making us susceptible to disorders and disease. So, why can’t we stop the bad cycle of indulging too much?
Apparently the link between drug addiction and food addiction is quite closer than we might think because both activate pathways in the brain that affect levels of the neurotransmitter dopamine (aka – the reward system). Get this: the same changes are seen in this pathway in both obese individuals and those that are addicted to cocaine, meth, and heroin! The higher preference there is for sugar correlated to a bigger preference for alcohol, cocaine and speed in rodent models.
Food also acts like a drug in that the more you are exposed to higher fat and higher sugar foods, the more your body will crave them (a ‘feed-forward’ system – ironic, right?). The higher your weight, the bigger the craving for high fat and high sugar foods. So you might wonder what happens if we actively choose to eat super healthy and stay away from junk (easier said than done considering we have pizza, burgers, and ice cream waiting at the back door). Even if you can withstand the higher cravings during ‘dieting’ – this usually leads to higher and longer periods of cravings, making it much easier to give in. Sometimes that salad just doesn’t do it for us, but those steak burritos across the street…..they just sound so yummy In studies done with animals, the longer time period of abstinence from high fat and high sugar foods caused their sugar cravings to increase, they had higher anxiety levels, they were more susceptible and higher tendency to show food-seeking behavior – you can see how this can become a never-ending cycle – like Lindsay Lohan’s frequent visits to rehab. These effects create the yo-yo dieting that is common in our society.
Similar to drug use, there are also withdrawal symptoms after abstaining from high fat/high sugar foods - emotionalism, anxiety, cravings (the neurological symptoms), but also physical symptoms like teeth chattering and tremors (shown in rodents). They mental and physical symptoms are attributed to changes that happen in the brain after exposure to these foods. One that I mentioned before: dopamine levels change and the body’s response to it are altered, but also changes in the receptors for endocannabinoids (think, marijuana), and changes in receptors for opioids. The more we eat junk food, the more we want it – risking health issues and obesity (and get this: the more obese a person is, the less likely they are to become addicted to drugs, because food fills that void). The changes that happen in the brain seem permanent; this is why many people gain the weight back that they lost years ago (so relapsing to bad behaviors doesn’t just happen after short-term healthy eating).
Evolutionarily, seeking out high fat and high sugar foods was crucial in times when food wasn’t readily available… so the problem is that while we have food everywhere now, our bodies haven’t really caught up.
Questions to think about:
1) Can we override the signals in the brain that tell us to seek more food?
2) How well does cognitive behavioral therapy work for overweight and obese patients?
3) To what extent can exercise reverse changes that happen in the brain and body that increase the drive to eat?
Forgetfulness… it happens to all of us. In the midst of our busy schedules we can forget appointments, the pesky errands on our to-do lists, ‘oh shoot I forgot to send Mr. Smith that email…’. But what about the memory loss that happens with dementia?
It is estimated that 5.4 million people suffer from Alzheimer’s disease (the most common form of dementia). Typically, most cases of Alzheimer’s are in people over the age of 65, and a 5th of those over 65 will die of Alzheimer’s related complications. You may even know a family member that has it because it is so prevalent. It’s thought that about 50% of people over the age of 80 years old will develop Alzheimer’s disease. It’s also tough to put a finger on what the cause is of this debilitating disease…. just getting older is a large factor. It’s been suggested that education level, amount of physical activity, healthy eating, and mindful activities can attribute to Alzheimer’s development. Even still, sometimes the healthiest most educated people can develop Alzheimer’s. There is a genetic component that seems to contribute to Alzheimer’s development, the ApoE gene; if someone has a certain form of the gene, the ApoE4 allele, their risk for Alzheimer’s is much higher. A normally functioning ApoE gene will help to clear beta-amyloid protein clumps in the brain. If the beta-amyloid doesn’t get cleared away it builds up and this is what leads to neuron death and ultimately the symptoms we see in Alzheimer’s patients. It seems that those people with the ApoE4 gene have an impaired mechanism to clear those protein clumps from beta-amyloid.
Treatment for Alzheimer’s is available, but the medications currently given cannot reverse the changes in the brain due to the beta-amyloid formation. They can help to slow the progression of the disease, but ultimately the patients still decline in cognitive function and their physical abilities.
There is good news though! Just a few weeks ago a study was published from the Landreth lab at Case Western in Science magazine with a potential breakthrough medication that may reverse the effects of beta-amyloid protein aggregation. The interesting thing is that this is a drug that has been used for the treatment of cancer, so it is already FDA approved for human ingestion. The study showed that levels of beta-amyloid in mice in the areas of the brain associated with cognitive decline in Alzheimer’s disease, there was a clearance of 40% within 72 hours. Even more exciting is that the mice had restored memory and cognitive function! The mice were also restored in their abilities to smell and build nests. This is a huge change from the currently prescribed meds that are not able to restore memory and physical abilities.
While this drug has not yet been approved for the treatment of Alzheimer’s disease, it is a promising new leap in the area of treatment for this debilitating disease. The future for better treatments of this disease seems promising and bright!