With the many sound bytes that you hear about in world and economic changes everyday, usually increases in prices and/or shortages in food and gasoline, I am happy to announce that effective July 2022, I have relocated my practice and as a result have reduced my fee for all psychotherapy and health coaching services. My new office location is 3490 SW 107 Court, Miami, 33165. My new fee is $165 per session hour. My fee for consultations is $65.
If you or someone who you know needs my services, you may reach me at 305-720-0237. You may also email me at drjosesandoval@gmx.com.
Meditating before running could change the brain in ways that are more beneficial for mental health than practicing either of those activities alone, according to an interesting study of a new treatment program for people with depression.
As many people know from experience, depression is characterized in part by an inability to stop dwelling on gloomy thoughts and unhappy memories from the past. Researchers suspect that this thinking pattern, known as rumination, may involve two areas of the brain in particular: the prefrontal cortex, a part of the brain that helps to control attention and focus, and the hippocampus, which is critical for learning and memory. In some studies, people with severe depression have been found to have a smaller hippocampus than people who are not depressed.
Interestingly, meditation and exercise affect those same portions of the brain, although in varying ways. In brain-scan studies, people who are long-term meditators, for instance, generally display different patterns of brain-cell communication in their prefrontal cortex during cognitive tests than people who don’t meditate. Those differences are believed to indicate that the meditators possess a more honed ability to focus and concentrate.
Meanwhile, according to animal studies, aerobic exercise substantially increases the production of new brain cells in the hippocampus.
Both meditation and exercise also have proven beneficial in the treatment of anxiety, depression and other mood disorders.
These various findings about exercise and meditation intrigued researchers at Rutgers University in New Brunswick, N.J., who began to wonder whether, since meditation and exercise on their own improve moods, combining the two might intensify the impacts of each.
So, for the new study, which was published last month in Translational Psychiatry, the scientists recruited 52 men and women, 22 of whom had been given diagnoses of depression. The researchers confirmed that diagnosis with their own tests and then asked all of the volunteers to complete a computerized test of their ability to focus while sensors measured electrical signals in their brains.
The researchers found that the depressed volunteers showed signaling patterns in their prefrontal cortex that are associated with poor concentration and focus.
Then the researchers had all of the volunteers begin a fairly rigorous, supervised program of sitting, followed by sweating.
To start, the volunteers were taught a form of meditation known as focused attention. Essentially entry-level mindfulness meditation, it requires people to sit quietly and think about their respiration by counting their breaths up to 10 and then backward. This practice is not easy, especially at first.
“If people found their thoughts wandering” during the meditation, and especially if they began to ruminate on unpleasant memories, they were told not to worry or judge themselves, “but just to start counting again from one,” said Brandon Alderman, a professor of exercise science at Rutgers who led the study.
The volunteers meditated in this way for 20 minutes, then stood and undertook 10 minutes of walking meditation, in which they paid close attention to each footfall.
Then they clambered onto treadmills or stationary bicycles at the lab and jogged or pedaled at a moderate pace for 30 minutes (with five minutes of warming up and five minutes of cooling down).
The volunteers completed these sessions twice a week for eight weeks. Then the researchers retested their moods and their ability to focus and concentrate.
There were significant changes. The 22 volunteers with depression now had a 40 percent reduction in symptoms of the condition. They reported, in particular, much less inclination to ruminate over bad memories.
Meanwhile, the members of the healthy control group also reported feeling happier than they had at the start of the study.
Objectively, the volunteers’ results on the computerized tests of their ability to focus and their brain activity also were different. The group with depression now showed brain cell activity in their prefrontal cortex that was almost identical to that of the people without depression. They could concentrate much better and hone their attention, attributes that are believed to help reduce stubborn rumination.
“I was quite surprised that we saw such a robust effect after only eight weeks,” Dr. Alderman said.
He and his colleagues theorize that the meditation and exercise may have produced synergistic effects on the brains of their volunteers.
“We know from animal studies that effortful learning, such as is involved in learning how to meditate, encourages new neurons to mature” in the hippocampus, he said.
So while the exercise most likely increased the number of new brain cells in each volunteer’s hippocampus, Dr. Alderman said, the meditation may have helped to keep more of those neurons alive and functioning than if people had not meditated.
Meditation also may have made the exercise more tolerable, he said, since some studies indicate that being mindful of your breathing and your body during workouts increases people’s enjoyment of the exertion.
“I’ve started meditating,” said Dr. Alderman, a long-time athlete.
Of course, this was a small study and the scientists did not follow their volunteers long term, so they do not know if any mood improvements linger. They also have no idea whether similar or even greater benefits might occur if someone were to run and then meditate or to practice both activities but on alternating days. They plan to study those questions in future experiments.
New research by investigators at Brigham and Women’s Hospital (BWH) suggests that bacteria living in the gut may remotely influence the activity of cells in the brain that are involved in controlling inflammation and neurodegeneration. Using pre-clinical models for multiple sclerosis (MS) and samples from MS patients, the team found evidence that changes in diet and gut flora may influence astrocytes in the brain, and, consequently, neurodegeneration, pointing to potential therapeutic targets. The team’s results are published this week in Nature Medicine.
“For the first time, we’ve been able to identify that food has some sort of remote control over central nervous system inflammation,” said corresponding author Francisco Quintana, PhD, an investigator in the Ann Romney Center for Neurologic Diseases at BWH. “What we eat influences the ability of bacteria in our gut to produce small molecules, some of which are capable of traveling all the way to the brain. This opens up an area that’s largely been unknown until now: how the gut controls brain inflammation.”
Previous investigations have suggested a connection between the gut microbiome and brain inflammation, but how the two are linked and how diet and microbial products influence this connection has remained largely unknown. To explore this connection further, Quintana and colleagues performed genome-wide transcriptional analyses on astrocytes — star-shaped cells that reside in the brain and spinal cord — in a mouse model of MS, identifying a molecular pathway involved in inflammation. They found that molecules derived from dietary tryptophan (an amino acid famously found in turkey and other foods) act on this pathway, and that when more of these molecules are present, astrocytes were able to limit brain inflammation. In blood samples from MS patients, the team found decreased levels of these tryptophan-derived molecules.
“Deficits in the gut flora, deficits in the diet or deficits in the ability to uptake these products from the gut flora or transport them from the gut — any of these may lead to deficits that contribute to disease progression,” said Quintana.
The research team plans to investigate this pathway and the role of diet in future studies to determine if the new findings can be translated into targets for therapeutic intervention and biomarkers for diagnosing and detecting the advancement of disease.
Research challenging the ‘cholesterol hypothesis’ concludes benefits from statin therapy have been exaggerated and ‘bad’ cholesterol isn’t the enemy.
Research challenging the ‘cholesterol hypothesis’ concludes benefits from statin therapy have been exaggerated and ‘bad’ cholesterol isn’t the enemy.
You may have heard there are two types of cholesterol.
One is good while the other is bad.
This “bad” cholesterol is called low-density lipoprotein cholesterol (LDL).
The idea that elevated LDL cholesterol contributes to numerous health problems, including cardiovascular disease, is the crux of the “cholesterol hypothesis.”
“Turns out, not so much,” says Dr. Robert Lustig, a pediatric endocrinologist the University of California, San Francisco.
In technical terms, bad cholesterol is believed to atherogenic, or it promotes the formation of fatty plaques in the arteries. That’s why numerous pharmaceutical drugs, namely statins, target this cholesterol.
But according to prevailing thought and new research, focusing on bad cholesterol may be bad medicine, or at least provide an argument against statin therapy.
Research published this week in the British Medical Journal (BMJ) suggests otherwise. And according to researchers, provides rationale to reevaluate heart health guidelines.
The research team — comprised of experts from seven different countries — evaluated data collected from 19 studies on a total of 68,094 older adults. The team was seeking to determine if LDL cholesterol is associated with death in the older adults.
According to the cholesterol hypothesis, it should directly relate. According to the BMJ study, it doesn’t.
Researchers say almost 80 percent of the participants in the studies who had high LDL cholesterol did not die because of their cholesterol level.
On the other hand, researchers discovered people with low levels of LDL cholesterol, or LDL-C, had the highest rates of death related to cardiovascular disease, the leading cause of death for both men and women in the United States.
“These findings provide a paradoxical contradiction to the cholesterol hypothesis,” researchers wrote. “The cholesterol hypothesis predicts that LDL-C will be associated with increased all-cause and [cardiovascular disease] mortality.”
Overall, the researchers — four of whom have published books criticizing the cholesterol hypothesis — say, “the benefits from statin treatment have been exaggerated.”
Those who have challenged the importance of LDL cholesterol say we’ve been measuring things incorrectly.
What researchers are learning is that cholesterol may not be a direct indicator of heart disease and total cholesterol — the accumulation of three types of fat in the blood — could be a useless metric.
Paying attention to triglycerides, however, might be the best number to monitor regarding heart health.
Lustig, an outspoken critic of the processed food industry, is one of those people. While not involved in the most recent BMJ research, said it proves that LDL cholesterol doesn’t matter.
But he’s not the first person to suggest so.
In the 1960s, there was a battle going on over what caused heart disease. There were two camps. One said sugar was the culprit while the other said dietary fat, particularly saturated fat, was the bad guy.
John Yudkin, a British physiologist and nutritionist, suggested sugar was to blame. Ancel Keys, an American scientist, pushed the dietary fat issue.
The two battled it out during the 1970s, but three major findings relegated fat as heart health enemy number one.
The first, Lustig says, was the issue of familial hypercholesterolemia, a genetic disease where people lacked an LDL receptor in their liver, causing them to die of a heart attack as early as their teenage years.
The second was that dietary fat raised LDL cholesterol.
“That is true. I’m not going to argue that,” Lustig said.
The third argument in the fat-is-bad argument was that elevated LDL levels in the larger population correlated with heart disease.
“That was the idea, and therefore fat was the problem, sugar wasn’t. Yudkin was thrown under the bus, died basically a forgotten man, and the low-fat hypothesis ruled the day, destroyed our diets, and basically caused the obesity and metabolic syndrome pandemic we now experience,” Lustig said in an interview with Healthline. “It turned out those three items, all of which were semi true, turned out to be irrelevant and were unrelated.”
Unfortunately, Yudkin didn’t have the body of evidence he does now, and Lustig says his argument that sugar, not fat, is the culprit remains true today.
While dietary fat does raise LDL cholesterol, there are two different kinds.
One, known as large buoyant LDL, is unrelated to heart disease, while small dense LDL cholesterol is the “true atherogenic particle.”
Carbohydrates, not fats, raise the small dense LDL cholesterol. Another byproduct of carbohydrates, sugar specifically, are triglycerides, which correlate better and predict heart disease, Lustig said.
“So we were using the wrong marker all along. It turned out the triglyceride was way worse. Triglyceride is basically what your liver does to sugar,” he said. “And again, sugar was the problem, Yudkin was right, and the food industry killed him.”
Below is a TEDx talk given by Mark Mattson, the current Chief of the Laboratory of Neuroscience at the National Institute on Aging. He is also a professor of Neuroscience at The Johns Hopkins University, and one of the foremost researchers in the area of cellular and molecular mechanisms underlying multiple neurodegenerative disorders, like Parkinson’s and Alzheimer’s disease.
I chose to include ‘Big Pharma’ in the title because that’s exactly what it is. There have been countless examples of the manipulation of published research at the hands of pharmaceutical companies in recent years. This is why Harvard Professor of Medicine Arnold Symour Relman told the world that the medical profession has been bought by the pharmaceutical industry. It’s why Dr. Richard Horton, Editor in Chief of The Lancet, recently stated that much of the sceintific literature published today is simply untrue. It’s why Dr. Marcia Angell, former Editor in Chief of The New England Journal of Medicine, said that the “pharmaceutical industry likes to depict itself as a research-based industry, as the source of innovative drugs. Nothing could be further from the truth.” And it’s why John Ioannidis, an epidemiologist at the Stanford University School of Medicine, published an article titled “Why Most Published Research Findings Are False” which subsequently became the most widely accessed article in the history of the Public Library of Science (PLoS).
I also chose to mention ‘Big Pharma’ because of Dr. Mattson’s comments towards the end of the video.
“Why is it that the normal diet is three meals a day plus snacks? It isn’t that it’s the healthiest eating pattern, now that’s my opinion but I think there is a lot of evidence to support that. There are a lot of pressures to have that eating pattern, there’s a lot of money involved. The food industry — are they going to make money from skipping breakfast like I did today? No, they’re going to lose money. If people fast, the food industry loses money. What about the pharmaceutical industries? What if people do some intermittent fasting, exercise periodically and are very healthy, is the pharmaceutical industry going to make any money on healthy people?”
Main Points Of The Lecture Above & The Science To Go With It
Mark and his team have published several papers that discuss how fasting twice a week could significantly lower the risk of developing both Parkinson’s and Alzheimer’s disease.
“Dietary changes have long been known to have an effect on the brain. Children who suffer from epileptic seizures have fewer of them when placed on caloric restriction or fasts. It is believed that fasting helps kick-start protective measures that help counteract the overexcited signals that epileptic brains often exhibit. (Some children with epilepsy have also benefited from a specific high-fat, low-carbohydrate diet.) Normal brains, when overfed, can experience another kind of uncontrolled excitation, impairing the brain’s function, Mattson and another researcher reported in January in the journal Nature Reviews Neuroscience.”(source)
Basically, when you take a look at caloric restriction studies, many of them show a prolonged lifespan as well as an increased ability to fight chronic disease.
“Calorie restriction (CR) extends life span and retards age-related chronic diseases in a variety of species, including rats, mice, fish, flies, worms, and yeast. The mechanism or mechanisms through which this occurs are unclear.”
Fasting does good things for the brain, and this is evident by all of the beneficial neurochemical changes that happen in the brain when we fast. It also improves cognitive function, increases neurotrophic factors, increases stress resistance, and reduces inflammation.
Fasting is a challenge to your brain, and your brain responds to that challenge by adapting stress response pathways which help your brain cope with stress and risk for disease. The same changes that occur in the brain during fasting mimic the changes that occur with regular exercise. They both increase the production of protein in the brain (neurotrophic factors), which in turn promotes the growth of neurons, the connection between neurons, and the strength of synapses.
“Challenges to your brain, whether it’s intermittent fasting [or] vigorous exercise . . . is cognitive challenges. When this happens neuro-circuits are activated, levels of neurotrophic factors increase, that promotes the growth of neurons [and] the formation and strengthening of synapses. . . .”
Fasting can also stimulate the production of new nerve cells from stem cells in the hippocampus. He also mentions ketones (an energy source for neurons), and how fasting stimulates the production of ketones and that it may also increase the number of mitochondria in neurons. Fasting also increases the number of mitochondria in nerve cells; this comes as a result of the neurons adapting to the stress of fasting (by producing more mitochondria).
By increasing the number of mitochondria in the neurons, the ability for nerons to form and maintain the connections between each other also increases, thereby improving learning and memory ability.
“Intermittent fasting enhances the ability of nerve cells to repair DNA.”
He also goes into the evolutionary aspect of this theory – how our ancestors adapted and were built for going long periods of time without food.
A study published in the June 5 issue of Cell Stem Cell by researchers from the University of Southern California showed that cycles of prolonged fasting protect against immune system damage and, moreover, induce immune system regeneration. They concluded that fasting shifts stem cells from a dormant state to a state of self-renewal. It triggers stem cell based regeneration of an organ or system. (source)
Human clinical trials were conducted using patients who were receiving chemotherapy. For long periods of time, patients did not eat, which significantly lowered their white blood cell counts. In mice, fasting cycles “flipped a regenerative switch, changing the signalling pathways for hematopoietic stem cells, which are responsible for the generation of blood and immune systems.”
This means that fasting kills off old and damaged immune cells, and when the body rebounds it uses stem cells to create brand new, completely healthy cells.
“We could not predict that prolonged fasting would have such a remarkable effect in promoting stem cell-based regeneration of the heatopoietic system. . . . When you starve, the system tries to save energy, and one of the things it can do to save energy is to recycle a lot of the immune cells that are not needed, especially those that may be damaged. What we started noticing in both our human work and animal work is that the white blood cell count goes down with prolonged fasting. Then when you re-feed, the blood cells come back. ” – Valter Longo, corresponding author (source)
A scientific review of multiple scientific studies regarding fasting was published in The American Journal of Clinical Nutrition in 2007. It examined a multitude of both human and animal studies and determined that fasting is an effective way to reduce the risk of cardiovascular disease and cancer. It also showed significant potential in treating diabetes. (source)
Before You Fast
Before you fast, make sure you do your research. Personally, I’ve been fasting for years, so it is something that comes easy for me.
One recommended way of doing it — which was tested by the BBC’s Michael Mosley in order to reverse his diabetes, high cholesterol, and other problems that were associated with his obesity — is what is known as the “5:2 Diet.” On the 5:2 plan, you cut your food down to one-fourth of your normal daily calories on fasting days (about 600 calories for men and about 500 for women), while consuming plenty of water and tea. On the other five days of the week, you can eat normally.
Another way to do it, as mentioned above, is to restrict your food intake between the hours of 11am and 7pm daily, while not eating during the hours outside of that time.
Bottom line, how you think about you’re diet is, in my opinion, one of the most, if not the most important part of staying healthy. How you think about what you are putting in your body is important, and I believe this will eventually be firmly established in the untainted, unbiased, uninfluenced medical literature of the future.
Below is a video of Dr. Joseph Mercola explaining the benefits of intermittent fasting. Here is a great article by him that explains how he believes intermittent fasting can help you live a healthier life.
