UCSF Health physicians have successfully treated a patient with severe depression by tapping into the specific brain circuit involved in depressive brain patterns and resetting them using the equivalent of a pacemaker for the brain.
UCSF is my medical alma mater, and I am proud to comment on their info graphic about need-driven deep brain stimulation (DBS). This is not only a good idea, it should spearhead a personalized wave of the future.
Your body’s metabolism is a great balancing act, and needs to be kept on an even keel, to maintain the stability of your internal environment. What is “good” at one time may be deleterious at another.
Good illustrations of this are insulin and thyroid hormone. Both too little and too much is deleterious.
Likewise, the need for DBS varies.. This was recognized by the designers of feedback-driven DBS. The amygdala is overactive when the depressive wave is greatest, triggering the deep brain stimulation. As the depressive wave lightens, the stimulation diminishes or stops.
Engineers are quite attentive to this idea. A similar feedback mechanism is used by implanted heart stimulators, or “ defibrillators“. if the heart slows down excessively, there is stimulation of the atrium to restore the proper rate. If the ventricle is ineffective, and fibrillates, it is given a shock which acts like rebooting your computer.
Chronotherapy, the administration of medication depending upon the time of day, is a kindred idea, illustrated by asthma. Wheezing attacks peak at night, when adrenaline and cortisol ebb, and so should the blood levels of the anti-asthmatic medication, theophylline.
Another illustration is the medication omeprazole, a proton pump inhibitor that reduces stomach acid. Reflux of this acid into the esophagus increases when you are recumbent and sleeping.. The need for the antacid is therefore greatest at night.
It is estimated that the effects of at least 50% of all medications would benefit by attending to the diurnal cycles. If your symptoms cycle with the sun, ask your doctor about your medications.
Lithium’s big claim to medical fame is it’s beneficial effect on manic depressive disorders in approximately 1/3 of the cases. It seems to benefit the manic phase more than the depressive phase, and its effect on isolated depression is uncertain.
A recent report states that lithium works by increasing CRMP 2, which has an effect on tubulin in nerve cells. This report has not yet been confirmed.
When lithium is effective, it must be given in a dose that is almost toxic. People taking this drug should have lithium levels on a regular basis, and be alert to its numerous side effects, diarrhea, lethargy, and the like. It may also have an adverse effect on thyroid function.
I started taking low doses of lithium orotate a while back because of the touted effects on memory, mitochondrial function, and the like. I thought that our hunter gatherer ancestors probably had some exposure to lithium from the Hot Springs present in many areas, and that maybe lithium was a physiologic necessity. Sodium and potassium are highly regulated ions in the cell membrane of all cells, I thought, so why should not lithium, a kindred element, have some effect there.
Lithium carbonate is the form that is used for treatment of manic depressive disease, and lithium orotate has not been well studied. When one starts taking a dietary supplement, it is hard to tell whether or not it has any effect. Our bodies are complicated, and even if something does have an effect, the bodies corrective mechanisms can nullify that effect, or even cause a reverse effect,
After further thought, I plan to start phasing out my lithium orotate. Maybe once a week would be a reasonable dosage, if at all. With irregular dosages, if I notice that I feel better on a day when I take lithium orotate, I might change my mind.
If you don’t know the signs of a stroke, you’re not alone. Thirty percent of people under the age of 45 don’t either. The key is to B.E. F.A.S.T. Learn how this acronym can help you save a life. The information in this video is accurate as of 9.17.21 and is for information purposes only. Consult your local medical authority or your healthcare practitioner for advice. Resources: Stroke: Causes and Prevention: https://cle.clinic/3hIHtab Stroke Signs & Symptoms: https://cle.clinic/3oLyQhc Stroke Risk Factors: https://cle.clinic/3hJ8r1s
More than 55 million people worldwide are living with dementia, a neurological disorder that robs them of their memory and costs the world $1.3 trillion a year, the World Health Organization (WHO) said on Thursday.
Preventing Dementia by healthful living habits such as good sleep, diet and exercise would certainly save lots of misery and expense, by preventing dementia. These same habits would also go a long way in preventing auto immune disease, diabetes and chronic stress.
Degenerative neurological diseases are particularly horrible. They affect the brain, the very essence of our humanity. Moreover, almost all of these conditions have no satisfactory treatment. Alzheimer’s, Parkinson’s, and Huntington’s disease come to mind.
Much more is known about the genetics of Huntington’s than any other aspect of the disease. The problem is due to CAG repeats, which either crowd out or distort the function of the Htt protein.
If a child of a Huntington family anticipates having children, intervention to prevent transmission, such as artificial insemination and eliminating any zygotes containing the Huntington Gene will prevent the children from inheriting the disease.
Huntington’s is considered to be inherited by a somatic dominant Gene. This gene codes for a number of CAG repeats in excess of the normal number, less than 35. However the number of CAG repeats tends to increase with each generation, and it is possible for parents with somewhat less than 35 repeats eventually to produce the disease in their offspring.
As in any degenerative brain disease, the focus of medical treatment is on neurotransmitters. This is because neurotransmitters can be studied and used as the basis of medical treatment that lessens the effects of the disease. In the case of Huntington’s, dopamine, glutamate and acetylcholine have all been implicated, although transmitter balance is probably more important, and changes with time.
Neural malfunction, however, is where the true pathology lies, and all neurons, especially those of the Corpus stratum and Cerebral Cortex contain Htt and are eventually involved, Leaving a shrunken brain that loses much of its substance and function.
The symptoms begin as a movement disorder, and initially was called Huntington Chorea, because of the abnormal “Dance-like” movements of affected individuals . Eventually, psychiatric, intellectual and other symptoms occur which span all areas of the brain.
Today, after swimming, I encountered a man whose brother has Huntington’s disease. So far he has been spared. He is part of a study of Huntington’s Disease Families. He denies knowing anything about his genetics, and indeed does not want to know, Nor would I in his situation, since nothing can be done to affect the basic progress of the disease.
Please refer to the accompanying meal clinic article for more information about Huntington‘s disease.
For many people, depression turns out to be one of the most disabling illnesses that we have in society. Despite the treatments that we have available, many people are not responding that well. It’s a disorder that can be very disabling in society. It’s also a disorder that has medical consequences.
By understanding the neurobiology of depression we hope to be able more to find the right treatment for the patient suffering from this disease. The current standard of care for the treatment of depression is based on what we call the monoamine deficiency hypothesis. Essentially, presuming that one of three neurotransmitters in the brain is deficient or underactive. But the reality is, there are more than 100 neurotransmitters in the brain. And billions of connections between neurons. So we know that that’s a limited hypothesis. Neurotransmitters can be thought of as the chemical messengers within the brain, it’s what helps one cell in the brain communicate with another, to pass that message along from one brain region to another. For decades, we thought that the primary pathology, the primary cause of depression was some abnormality in these neurotransmitters, specifically serotonin or norepinephrine. However, norepinephrine and serotonin did not seem to be able to account for this cause, or to cause the symptoms of depression in people who had major depression. Instead, the chemical messengers between the nerve cells in the higher centers of the brain, which include glutamate and GABA, were possibilities as alternative causes for the symptoms of depression. When you’re exposed to severe and chronic stress like people experience when they have depression, you lose some of the connections between the nerve cells. The communication in these circuits becomes inefficient and noisy, we think that the loss of these synaptic connections contributes to the biology of depression. There are clear differences between a healthy brain and a depressed brain. And the exciting thing is, when you treat that depression effectively, the brain goes back to looking like a healthy brain, both at the cellular level and at a global scale. It’s critical to understand the neurobiology of depression and how the brain plays a role in that for two main reasons. One, it helps us understand how the disease develops and progresses, and we can start to target treatments based on that. We are in a new era of psychiatry. This is a paradigm shift, away from a model of monoaminergic deficiency to a fuller understanding of the brain as a complex neurochemical organ. All of the research is driven by the imperative to alleviate human suffering. Depression is one of the most substantial contributors to human suffering. The opportunity to make even a tiny dent in that is an incredible opportunity.
Opportunities for enhancing brain health across the lifespan
Published online by Cambridge University Press: 22 March 2021
As we age, there are characteristic changes in our thinking, reasoning and memory skills (referred to as cognitive ageing). However, variation between people in the timing and degree of change experienced suggests that a range of factors determine individual cognitive ageing trajectories. This narrative review considers some of the lifestyle factors that might promote (or harm) cognitive health. The focus on lifestyle factors is because these are potentially modifiable by individuals or may be the targets of behavioural or societal interventions. To support that, the review briefly considers people’s beliefs and attitudes about cognitive ageing; the nature and timing of cognitive changes across the lifespan; and the genetic contributions to cognitive ability level and change. In introducing potentially modifiable determinants, a framing that draws evidence derived from epidemiological studies of dementia is provided, before an overview of lifestyle and behavioural predictors of cognitive health, including education and occupation, diet and activity.
LOS ANGELES — Modifying 12 risk factors over a lifetime could delay or prevent 40% of dementia cases, according to an updated report by the Lancet Commission on dementia prevention, intervention and care presented at the Alzheimer’s Association International Conference (AAIC 2020).
Twenty-eight world-leading dementia experts added three new risk factors in the new report — excessive alcohol intake and head injury in mid-life and air pollution in later life. These are in addition to nine factors previously identified by the commission in 2017: less education early in life; mid-life hearing loss, hypertension and obesity; and smoking, depression, social isolation, physical inactivity and diabetes later in life (65 and up).
Schneider and commission members recommend that policymakers and individuals adopt the following interventions:
Aim to maintain systolic blood pressure of 130 mm Hg or less from the age of 40.
Encourage use of hearing aids for hearing loss and reduce hearing loss by protecting ears from high noise levels.
Reduce exposure to air pollution and second-hand tobacco smoke.
Prevent head injury (particularly by targeting high-risk occupations).
Limit alcohol intake to no more than 21 units per week (one unit of alcohol equals 10 ml or 8 g pure alcohol).
Stop smoking and support others to stop smoking.
Provide all children with primary and secondary education.
Lead an active life into mid-life and possibly later life.
Reduce obesity and the linked condition of diabetes.
We ARE our brains. Reduce the function of any other organ, and we may be sick, but reduce the function of the brain, and WE have changed.
PROGRESSIVE LOSS of brain function is called DEMENTIA. A sudden, temporary (if the cause can be found) is called Delirium. A variety of bad things can cause dementia, such as infections (AIDS), toxins (lead, mercury), chemicals (alcohol), traumatic (CTE from football), diet deficiencies (B12, folic acid), Endocrine deficiencies (thyroid),Psychiatric problems (depression), drugs, and Vascular problems.
The Preceding article on dementia discussed APATHY, as opposed to the somewhat similar DEPRESSION, as a warning sign for SVD, or small blood-vessel disease. SVD is the most common VASCULAR cause of Dementia.
The most common overall cause of Dementia, especially in old age, is ALZHEIMER’S disease (AD). “Senior Moments” are so common as to be a cliche. But this problem is not limited to old age. My 3-year-old Grandson came crying to me that he lost his favorite toy. “Where was it when you last saw it”?, I asked. “It was in my hand” he answered.
He had laid it somewhere, unthinkingly. You can’t remember something unless you ENCODE it. You must be paying attention to, be “mindful” of an action if you are to remember that action.. You will not remember where you put your glasses if you wander around in “default mode”, daydreaming, preoccupied. Everybody occasionally forgets a name, or item which hangs on “the end of my tongue”.
These things, especially “short term memory” do DETERIORATE AS WE GET OLDER. It is common to wonder if we, or a loved one. are getting Alzheimer’s disease, as our mental powers wane.It is often difficult to distinguish the normal forgetfulness of age from DEMENTIA, including Alzheimer’s Disease (AD) It might be a source of REASSURANCE to realize that if you are worried about getting AD YOURSELF, you almost certainly don’t have it; It takes a lot of mental functioning to contemplate that possibility.
Most often, you will be wondering about the possibility in a loved one having AD. There are 2 ideas that I ran across in my reading that might help you do a little evaluation Yourself.
BCGuidelines.ca has a 21 item questionnaire that you can score yourself. 4 points or less is considered normal, so common is forgetfulness. 5-14 points suggests mild cognitive impairment. 15 or more points suggests Dementia, of which AD is the most common type.
The test I really liked was the “Clock Test”. In this test, you draw a large circle. You then ask your loved one to draw a clock, with all the numbers and hands that will indicate 10 minutes after 11. If it is drawn correctly, you can with reasonable certainty EXCLUDE Dementia.
If incorrect, further tests are warranted. I consulted with a Neurologist regarding a friend of mine who has marked memory loss, but is very sweet, is physically capable, takes care of herself personally, doesn’t wander around, has no apparent anxiety, depression or other psychological problems.
I asked if it was reasonable to just watch without any medical intervention. The neurologist said that she should have a blood test, a metabolic panel, TSH (thyroid), LFTs, folic acid and B12 tests, and a CT to rule out NPH (normal pressure hydrocephalus). It is rare to find anything treatable, but a shame to neglect it if present.
If you do see a doctor about a Spouse or Parent with possible dementia, you might request that they discuss the possibilities with you, but ask them not to write the diagnosis of “Alzheimer’s “ in the chart. Private Assisted Living Homes CHARGE A LOT MORE for that Diagnosis– locked facilities, more personnel and the like. BDNF- brain derived neurotrophic factor- can fend off Dementia.
That is the good news. The bad news is that it takes effort and discipline to increase your level od BDNF.; I’m sure medical science is hot on the trail of a pill. But until then, our old friends, Sleep, Diet and Exercise ride to the rescue. Sleep, both N3 and REM stages, increases BDNF. Dietary polyphenols and butyrate increase BDNF. exercise of all kinds will do it.
The BDNF gene codes for the BDNF protein, which promotes the survival, expansion, and differentiation of Neuronal stem cells, and promotes neuronal PLASTICITY, neuronal response to experience. Grit your teeth and develop the HABIT of exposing your Postmodern Body to 3 of the most ICONIC and NATURAL things mandated by Evolution, Treat your Body to the Health-giving Benefits of SLEEP, DIET and EXERCISE!
Empowering Patients Through Education And Telemedicine