Cobbers on the Brain

The aging process is one we’ve studied as a people for as long we’ve existed. And extending our lives has always been a major motivation in those studies. Our current understanding of aging at a cellular basis is one of oxidative stress and mitochondrial damage. Over time, our cells create more and more reactive oxygen species (ROS) that cannot be broken down before doing their damage, which lead to the generation of more ROS. I’ll break down the concept and introduce a few interesting ideas from our class discussions.

The mitochondria, the most well-known organelle in the cell. It gets its memorable nickname the “Powerhouse of the Cell” from its function, creating energy. The mitochondria can be thought of as a factory, but it can be better visualized as a furnace. Just like any bomb or engine, sugar breakdown is a combustion reaction. A carbohydrate reacts with oxygen and breaks down to water, carbon dioxide, and energy. So in the mitochondria, sugar is broken down and the heat/energy given off is utilized to generate energy molecules for the cell. However, this process isn’t perfect. Instead of becoming carbon dioxide, the oxygen molecules can be changed to reactive oxygen species, like superoxide.
These ROS are dangerous, a given with the name reactive. They damage DNA, proteins, and membranes. The damaged DNA works less efficiently and increases the chances for mutations. The proteins that are damaged dysfunction and/or accumulate. Membrane damage along with protein damage are important for their impact on the mitochondria. The ROS generated by the mitochondria, turn around and cause it to generate even more ROS. This positive-feedback loop would lead to the accumulation of a lethal amount of ROS. Our body takes care of this with proteins that neutralize ROS. As stated above, ROS damage proteins as well. Over time, our body loses the fight against ROS generation. Leading to disease and aging.
How does this concept apply to us? Calories basically equate to energy for the mitochondria. Meaning that, calories, by virtue, lead to ROS as well. The oxidative stress of calorie consumption is a natural part of life and the aging process. Overnutrition exaggerates that stress. When our body takes in too many calories over a short or extended period of time, it generates more oxidative stress. How relevant is this to the aging process? That’s where we need to learn more.
There is interesting evidence in support of that. Rats have been shown to live longer if their amount of proteins neutralizing ROS are increased. That doesn’t hold true 100% of the time, though. Sometimes the opposite effect happens with similar proteins. The current hypothesis is that ROS are damaging, however, they do have a necessary function in the cell that can be disrupted. The most interesting idea I came across was that reducing caloric intake extended life span.
It has been shown in many experiments with varying mammals that reducing caloric intake by 30-50% below what the animals would eat if they had no restrictions, leads to a significant extension in lifespan. This idea is very interesting for thinking about extending life, but it’s also very applicable on the opposite side of the spectrum, overeating and reduced lifespan. Overeating is obviously a concern in many countries throughout the world and its effects on aging and possible controlling those effects calls for more investigation. Life-extenstion is also very interesting, but those studies called for reduced feeding during development. Reducing calories that far is hard to do in the first place, but its negative effects on even an adult’s body wouldn’t be worth any hopeful benefit in lifespan. Going forward, it will be interesting to see how the role of oxidative stress and overnutrition becomes a factor in preventing and treating illness.

Tobacco and weed have both been used for thousands of years by many different peoples, and yet the past 100 years in America have been a time of equating cannabis to heroic and other narcotics. Odd that tobacco which has been shown to strongly associate with cancer and other health issues many years ago (what a struggle that was against the cigarette corporations) is legal in today’s society when weed illegal even though it’s identified negatives are far below that of tobaccos. Some of the stereotypical negative effects cited by the first website to appear in google include memory issues, reduced reaction time, lower iq, impaired thinking, relationship issues, antisocial behavior, financial difficulties, increased welfare dependence, and greater chance of being unemployed. The effects are marijuana are poorly understood because it hasn’t been studied in the US due to being treated like a narcotic rather than potential medicine. So where do these drug effects come from if not from scientific studies? That’s the story of why weed is illegal.
It’s true that weed has negative effects. One you’re smoking, bad no matter what and damages the lungs. Two you’re introducing high amounts of outside chemicals to your body, may not harm too bad but can’t really be good for you either. And thirdly, weed and other drugs should never be used by those still in development, youth. However, side effects like relationship issues, antisocial behavior (stealing, lying) and the financial issues and welfare have a basis outside of science. Those trends might be seen in today’s world, but they were determined to be true long ago.

Marijuana was legal in the use into the 1900’s, however, the Mexican revolution occurred in 1910. Following that event, many Mexican immigrants began to cross the border and with them came weed. Pretty much immediately, state governments began criminalizing marijuana (just like heroin) due to it’s association with the Mexican immigrants. Newspapers publicizing this said things like “Marihuana influences Negroes to look at white people in the eye, step on white men’s shadows and look at a white woman twice.” At the time, regulating drugs like the FDA does now wasn’t constitutional, which is why an amendment was required to ban alcohol. The next stage in our story involves that, prohibition ending in 1933. After prohibition ended Harry J. Anslinger (head of federal bureau of narcotic) being an ambitious man sought to expand his influence by demonizing weed. Using racist publications already in place to justify its demonization and coming up with own, like “….the primary reason to outlaw marijuana is its effect on the degenerate races”. In the end, he was able to bring enough “evidence” to Congress from various racist journals and many from his friend William Hearst, who was the owner of a chain of newspapers with a hate for Mexicans. He was able to convince Congress to pass tax penalties on marijuana against the wishes of Dr. William C. Woodward, Legislative Council of the American Medical Assoc. The doctor called for more primary research before this decision but was ignored and the Marijuana Tax Act of 1937 was passed.
The tax act was found unconstitutional years later, however, the Controlled Substances Act in the 1970’s struck weed down once again. Nixon and the war on drugs, we now know it was resounding failure that we still cling too. Regardless, when the three classes of drugs were defined, weed was placed in schedule 1 initially so that a commission appointed by Nixon could determine its danger. The commission recommended removal from schedule 1 and possibly not consider it illicit at all. Nixon completely ignored this and classified it as schedule 1. Why would Nixon do this though? Not shocking that it was a shady political power move (no way Nixon). Nixon had two main political enemies in America, the Blacks and the Anti-War hippies. As one of Nixon’s aides (John Ehrlichman) opened up about, you can’t just target the pacifists and blacks directly, you have to punish them indirectly. In this case, criminalize the main drugs of use of these populations so that raids and busts can be used to disrupt political organization against him. This racist and political use of drug enforcement continues to this day, just look up the weed usage rates by race and the weed arrest rates by race. I bet you can guess you gets off easy and who doesn’t.
 

Short answer, overall not signifiantly. More complicated answer is that in some individuals in the obese population, leptin might help with the return of normal weights.
Leptin is a hormone that is secreted by fat cells in your body that signal for the brain to have a decrease in appetite. Because of this, abnormal production of this hormone has been associated with obese individuals.
Specifically in the body, leptin interacts with specialized leptin receptors to inhibit excess feeding. In obese individuals though we see very highly elevated levels of this hormone. So why isn’t it working?
Well, in the typical Western high-fat diet, both rodents and humans have shown in various studies to demonstrate a non-response to leptin. This is a problem for being able to use leptin as a weight-loss hormone, as the already high levels of this hormone in obese individuals are already having no effect.
But, that doesn’t mean that looking into further uses for leptin aren’t going to prove beneficial. Although many obese individuals have high levels of leptin, there is about 10% of obese individuals that have very low levels of leptin instead.
In these individuals, there is potential therapies akin to insulin treatment of patients with type 2 diabetes in the form of leptin therapy. In these individuals with truly low levels of leptin, this therapy has shown to induce a sustained increase in weight loss.
This is good news to show that although leptin therapy is not for everyone, if you are overweight or obese it might be well worth it to go get a check up to view your blood-leptin levels to see if this is a potential reason for your obesity.

We’ve all seen the Lays commercials where they “Bet You Can’t Eat Just One” of their amazing chips. And it’s true. It is really difficult to eat just one chip. We call them addicting, just like chocolate or cookies or your favorite flavor of ice cream.
When we say this, we are usually joking. Nobody shoots up Lays potato chips or has to go to potato-chip rehab to quit their addiction. But what if I told you that food addiction is real? As real as drug or nicotine or alcohol addiction?
Well, it is. But to understand how food can be addicting, we need to understand how addiction works in the first place.

The Basis of Addiction

Addicting things – alcohol, nicotine, drugs, sex, exercise, food – are addicting because they make you feel good. They do this by mimicking or causing the release of “feel good” chemicals in your brain like dopamine or endorphins.
In the case of dopamine, substances can cause the release of dopamine in your brain, which binds to dopamine receptors. Other drugs can bind dopamine receptors themselves. Either way, the same “feel good” effects are produced.
When your brain goes through this a lot, it starts to become resistant to it, which we call tolerance. Your brain develops tolerance by decreasing the number of dopamine receptors in your brain, so that you have to do more of the thing that makes you happy to reach the same level of happiness.
This is the common thing that occurs in drug and alcohol use, where your body pushes you to use or consume more and more to get the feelings that cause you to use in the first place.
This same effect can occur with the opioid system of the brain, which is normally activated by endorphins (the feel-good chemical released during exercise), but artificially stimulated by opiate drugs like painkillers or heroin.
But how is any of this related to food?

Food and Addiction 

Everybody knows that fat and sugar taste good, but it’s more than just flavor that makes them addictive. There have been many studies that simulate overeating of fatty or sugary (or fatty AND sugary) foods in mice and how that affects their brains.
One effect seen is a decrease in the number of dopamine receptors with subsequent increases in sugar intake, just like the reduced number of receptors and increased use that we see in drug tolerance.
Additionally, scientists have found a decrease in the number of dopamine receptors in obese humans that correlates with their weight. So, the higher the weight, the less dopamine receptors they have. This means that they would need to consume larger amounts of sugary and fatty foods to elicit the same effect as those foods had in the past.
Another result is the activation of the opioid system caused by sugar intake. When rats were taken off of their sugary diet, they exhibited the same withdrawal symptoms that are typical of opiate drug withdrawals.
Rats who had been on a high-fat diet would traverse a painful and difficult terrain to get to high-fat foods rather than eat low-fat foods that were easily accessed.
All of these results indicate that fatty and sugary foods are, in fact, addicting.
 

Social Implications

So, since fat and sugar are addicting, it’s not my fault if I eat too much of them, right? Because I’m an addict and it’s out of my control?
Not quite.
Yes, these things are addicting. But the addiction does not just hit you out of the blue. It occurs as a result of over-consumption of fatty and sugary foods, and perpetuates continued over-consumption. So, that means I should never eat anything with fat or sugar, right?
Again, not quite.
Rats who had been consuming a lot of fat and sugar and then were not allowed to fat and sugar binged and relapsed as soon as they were allowed access to fatty and sugary substances. So cutting yourself off completely will likely lead to extreme overconsumption and relapse into unhealthy habits.
So, as with everything that has to do with a healthy lifestyle, consume them in moderation. A few potato chips and a little bit of chocolate won’t make you a full-blown addict, but too much will, so it is important to be aware of how much you consume and what’s going on in your brain in order to help yourself to live a healthy lifestyle.

Autism is a very common condition. This disorder is characterized by abnormal social behavior and communication. Autism is often caused by genetic factors, however, environmental factors also play a significant role. There are a large number of risk factors that increase the chances of a child developing autism. Some of these include:

• Viral infections during pregnancy
• Heavy metals
• Zinc deficiency
• Problems with melatonin synthesis
• Stress (before or after birth)
• Maternal diabetes
• Gastrointestinal irregularities
• Older parents
• Psychiatric drugs

It should be noted that vaccines are not on this list. Vaccinations do not increase the chances of a child developing autism.
Anyway, the risk factors listed above correlate with higher levels of autism. Genetics also play a role, but these factors somehow cause autism by altering brain development before or after birth.
So how does all this cause autism? Well it has to do with zinc and the immune system. Low zinc levels in the brain are correlated with autism (and might be a cause). Autism may also start with abnormalities in the immune system. There is not one cause of autism. Genes and the environment both play a role in this complicated disease.
Where do these abnormalities with the immune system and zinc levels come from, and what do they do?
Low zinc levels can be caused by a variety of factors. First there is genetics, deletions or mutations in certain genes can cause very low levels of zinc in the body. Gastrointestinal problems can also cause very little zinc to be absorbed into the body. There is also malnutrition (of either the mother or the baby). Heavy metals, especially copper, can also interfere with zinc adsorption in the body.
Immune system deficiencies also have a variety of causes. First of all, zinc deficiency can cause the immune system to not develop properly. Also, genetics can cause abnormalities in the immune system. These abnormalities can also be caused by many of the risk factors listed above such as toxins, stress, psychiatric drugs (taken by the mother), parental age (both parents), and melatonin deficiency.
Melatonin deficiency can be caused by low levels of Zinc. This causes the disturbed sleep patterns seen in autistic children and as stated above has negative effects on the immune system.
Autistic people also have some differences in how synapse are formed. For example some synapses have scaffolding proteins called Neurexin and Neurolinin. These proteins hold the two ends of the synapse together so signaling can occur. If these scaffolding proteins do not work right the signaling molecules may have a hard time getting to their receptors.  Some people with autism have mutations to the genes that code for these proteins rendering them nonfunctional. Low zinc levels can also cause these structural irregularities. These structural irregularities can lead to improper signaling, which leads to the symptoms of Autism.
Overall, autism in an incredibly complicated disease. It is widespread and still not fully understood. Still there is progress being made. Understanding what is happening the brain will help medical professionals make better treatments that can improve the lives of autistic people.