The Human Operating Manual

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Pain and Addiction

To be completed

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Reminder: Not medical advice, consult doctor before, etc.

What is the general understanding of pain and addiction?

Complications for the person, their family, and the public perception

How to think about recovery, management, and responsibility without distributing blame (the emotionally charged aspect of this topic makes it hard to work on recovery without divisiveness). 

Each condition to address:

  •  What is it?
  • What may cause it and what are the commonalities between sufferers?
    • Endocrine
    • Anatomy/physiology
    • Environmental
    • Evolution/anthropology
    • Fetal development
    • Maternal/paternal health before conception
    • Genetics/epigenetics
    • Immune system
    • Nervous system
    • Psychology
  • What are some potential ways of managing symptoms?
    • Breathwork
    • Sleep and Circadian Rhythm
    • Nutrition
    • Trauma recovery
    • Social/Communal integration
    • Exercise
    • Purpose
    • Environment tailored
    • Tools: eustress

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Depression

Nutrient Power Notes

Typical symptoms include chronic sadness, feelings of worthlessness or guilt, social withdrawal, agitation, problems with concentration, and difficulty sleeping. Depression is a broad term used to describe a variety of medical conditions, including dysthymia, bipolar disorder, cyclothymic disorder, substance-induced mood disorder, seasonal affective disorder, and postpartum depression.

Biochemical Classification of Depression

Most depressives in the undermethylation biotype exhibit classic symptoms of low serotonin and report improved moods after serotonin-enhancing SSRI medications. In contrast, the folate deficiency biotype is associated with elevated serotonin and dopamine activity and intolerance to SSRI medications. High copper depressives have a strong tendency for reduced dopamine and elevated norepinephrine activity. Persons in the pyrrole biotype experience a nasty double deficiency of serotonin and GABA, which is the chief inhibitory (calming) neurotransmitter in the central nervous system. A serious toxic metal overload can impair the blood-brain barrier, disable key antioxidant proteins in the brain, damage the myelin sheath, and alter the concentrations of certain neurotransmitters.

  • Undermethylation: Reduced serotonin, dopamine
  • Folate deficiency: Elevated serotonin, dopamine
  • Copper overload: Elevated norepinephrine
  • Pyrrole disorder: Reduced serotonin, GABA

Undermethylated Depression

Approximately 38% of individuals in his depression database exhibit undermethylation as their dominant chemical imbalance. These persons appear to be highly sensitive to the methyl/folate ratio in the brain. They thrive on SAMe, methionine, and other powerful methylating agents but are strikingly intolerant to folates that also promote methylation.

Important indicators of this syndrome include a whole blood histamine level above 70 ng/ml and a depressed SAMe/SAH ratio in combination with key symptoms and traits such as OCD tendencies, seasonal allergies, and a history of perfectionism.

Methylation therapy for low-serotonin depressives is unique because of the need to limit folate intake that would increase production of SERT and reduce serotonin activity. The nutrient factor with the greatest positive impact for treatment of this depression biotype is direct methylation, either in the form of SAMe or the amino acid methionine.

Folate, choline, DMAE, and pantothenic acid supplements must be avoided since they increase chromatin acetylation and SERT levels. A high percentage of these patients exhibit low stores of calcium, vitamin D, and magnesium and thrive on supplements of these nutrients. In addition, nutrients that enhance synthesis of serotonin can be helpful (e.g., tryptophan, vitamin B-6, 5-HTP). Augmenting nutrients include vitamins A, C, and E.

Symptoms and Traits – Undermethylated Depression

  • Good response to SSRIs
  • Good response to SAMe, methionine
  • Adverse reaction to folic acid
  • High inner tension
  • Obsessive-compulsive tendencies
  • History of perfectionism
  • Self-motivated
  • Seasonal inhalant allergies
  • Good response to antihistamines
  • High libido
  • Low tolerance for pain
  • High fluidity (tears, saliva, etc.)
  • Very strong-willed
  • Competitiveness in sports
  • High suicidal tendency
  • Addictiveness
  • Sparse chest/leg/arm hair
  • Calm demeanor
  • Denial of depression
  • Frequent headaches
  • Family history of high accomplishment
  • Noncompliance with therapies
  • Rumination about past events
  • Oppositional defiance as child

Most undermethylated depressives exhibit low levels of homocysteine, but others may exhibit elevated levels. Since methylation therapy tends to elevate this biochemical, some patients must have treatment to normalize homocysteine levels prior to use of SAMe or methionine. In most cases, supplementation with serine and vitamin B6 for a few weeks can bring homocysteine down to a safe level. Experience with hundreds of undermethylated depressives has confirmed that folates, choline, manganese, copper, and DMAE tend to worsen their depression and must be strictly avoided.

Charles – 52 (Undermethylation):

  • Despite impressive career and financial successes, he had been depressed for more than 15 years with persistent thoughts of suicide. He reported that depression didn’t affect his work performance but was causing problems in his second marriage.
  • Symptoms of undermethylation included hay fever, high libido, internal anxiety, frequent headaches, and sparse hair on his chest, arms, and legs. Charles reported that Prozac, Zoloft, and Paxil all lessened depression, but side effects including a loss of sex drive, nausea, and a worsening of the headaches caused him to stop these medications.
  • His lab work revealed an extreme elevation of blood histamine (142 ng/ml), a mild elevation of urine pyrroles, and low-normal homocysteine.
  • His treatment consisted of SAMe, methionine, zinc, serine, calcium, magnesium, and vitamins A, B-6, C, D, and E.
  • Charles complained of a lack of progress after two months of treatment, but he reported improvement during month 3. After 12 months of treatment, he returned for testing and stated that his depression had been nearly gone for several months.

Julie – 42 (Undermethylation):

  • At age 16, she was diagnosed with oppositional-defiant disorder. She reported intermittent depression since her first marriage at age 19. She said her school grades were excellent until high school when she became more interested in boys than academics.
  • Episodes of chronic depression, especially in late spring and early fall. She had worked as a hair stylist and a waitress, and she was presently a sales clerk in a large department store. She reported several symptoms of undermethylated depression, including a shopping disorder, habitual cigarette smoking, sensitivity to ragweed and grasses, and a good response to antihistamines. Julie had tried three separate antidepressants but claimed none were effective.
  • Elevated blood histamine level of 82 ng/ml. Julie had limited funds and decided she couldn’t afford to take SAMe, a relatively expensive supplement. Her treatment involved high dosages of methionine, calcium, and magnesium together with zinc, vitamins B-6, C, D, and E, and chromium.
  • Julie returned for a follow-up evaluation after 6 months and reported that her depression was gone but that she still had problems with allergies and shopping binges.

A significant number of undermethylated depression patients exhibit some degree of pyrrole disorder. Many persons with this combination of imbalances exhibit high accomplishment throughout life, but report extreme internal anxiety and poor stress control along with depression. Since both undermethylation and pyrrole disorder are associated with low serotonin activity, depression is usually more severe in these cases and also more likely to report suicidal ideology.

Many persons suffering from undermethyated depression have two traits that make successful treatment difficult. First of all, they have an innate tendency for noncompliance with any medical treatment. Some admit they won’t take aspirin during a headache, even though they know it would help them. The second trait is a tendency to deny depression, even when the problem is severe.

Folate Deficiency Depression

Most report anxiety in addition to depression, and about 20% have a history of panic disorder or anxiety disorder. With very few exceptions, these persons report intolerance to SSRI antidepressants and antihistamines. A high percentage are noncompetitive persons who complain of chemical and food sensitivities but deny hay fever and other seasonal allergies. Despite their suffering, a surprising number are caring, generous persons with a history of volunteer work. The incidence of ADHD and academic underachievement is about three times higher than that observed for the undermethylated biotype.

Symptoms and Traits – Low-Folate Depression

  • Improvement after folate therapy
  • High anxiety and panic tendency
  • Adverse reaction to SSRIs
  • Improvement after benzodiazapines
  • Food and chemical sensitivities
  • Absence of seasonal allergies
  • Dry eyes and mouth
  • Low libido
  • High artistic abilities and interest
  • Hirsutism (males only)
  • Nervous legs, pacing
  • Sleep disorder
  • Noncompetitive in sports, games
  • Underachievement in school
  • Hyperactivity
  • High pain threshold
  • Upper body/head/neck pain
  • Adverse reaction to SAMe, methionine
  • Estrogen intolerance
  • Copper intolerance

Laboratory indications of low-folate depression include whole blood histamine below 40 ng/ml, an elevated SAMe/SAH ratio, low serum folate, and an absolute basophil count below 30.

Nutrient therapy for this biotype is focused on building up folate stores aimed at increasing acetylation of chromatin. Typical treatment formulations for low-folate depression include the following:

  • Folic or folinic acid
  • Vitamin B-12
  • Niacinamide, choline, DMAE, and manganese that reduce dopamine synaptic activity
  • Zinc, PLP, and vitamin B-6, which tend to increase GABA levels
  • Augmenting nutrients, including vitamins C and E

It is also important to avoid supplements of tryptophan, 5-HTP, phenylalanine, tyrosine, copper, and inositol in treating these individuals. Originally, folic acid dosages exceeding two mg/day were routinely prescribed to combat low-folate depression. However, folinic acid more efficiently passes the blood-brain barrier, enabling lower folate dosages for this depression biotype.

Marilyn – 36 (Low folate):

  • Poor academics through elementary and high school despite an IQ of 132 and motivation to succeed. She was diagnosed with ADD in the fourth grade and took Ritalin until eighth grade (caused appetite suppression and weight loss).
  • Depression at 20 and failure to improve symptoms with Zoloft (gave a panic attack), several other SSRIs, until Klonapin (benzo) lessened anxiety.
  • Chemical sensitivities, problems concentrating, dry eyes, low libido, and chronic neck pain. She reported taking Benedryl on one occasion and feeling “wired” and agitated.
  • Marilyn’s histamine tested at 16 ng/ml, and she was treated with high doses of folic acid, vitamin B-12, and niacinamide. Other prescribed nutrients included zinc, DMAE, manganese, chromium, and vitamins B-6, C and E, and she was urged to continue her Klonapin medication for several months.
  • Marilyn complained of heightened anxiety after two weeks of therapy but reported significant improvement in depression and anxiety (but not chemical sensitivities) at a 4-month follow-up visit. Continued for 6 years and says 95% better.

Karl – 28 (Low Folate):

  • Successful businessman, below-average student, happily married. Karl said he had experienced brief episodes of depression as a teen, but severe anxiety, depression, and a sleep disorder developed at age 25.
  • Prozac provided some benefit but had to be discontinued due to nausea and headaches. Treatment with Paxil, Zoloft, and Celexa (SSRI medications) resulted in heightened anxiety and depression.
  • Karl exhibited several symptoms of the low-folate biotype, including low libido, eye dryness that prevented wearing contact lenses, proficiency in water color painting, and thick hair on his chest and back.
  • Karl’s blood histamine level was 31 ng/ml, confirming his low folate status. His treatment centered on high doses of folic acid, vitamin B-12, and niacinamide. In addition, he received zinc, manganese, GABA, magnesium, DMAE, and vitamins B-6, C, and E. Karl has continued his nutrient therapy for several years and reports that he is quite well.

Low folate biotypes are at risk of suicidal thinking and behavior with SSRI antidepressants. School shootings have been associated with these drugs.

Hypercupremic Depression

About 17% of depression patients exhibit hypercupremia or elevated copper (Cu) as their dominant chemical imbalance. The vast majority (96%) of persons with this biotype are women, with the first episode of depression typically occurring during a hormonal event such as puberty, childbirth, or menopause. In addition to depression, characteristic symptoms include severe anxiety, sleep disorder, hormone imbalances, hyperactivity in childhood, skin sensitivity to metals and rough fabrics, ringing in the ears (tinnitus), and intolerance to estrogen, shellfish, and chocolate.

Norepinephrine elevations have been associated with anxiety/panic disorders, sleep problems, paranoia, and, in severe cases, psychosis. Copper-overloaded depressives usually report that serotonin-enhancing antidepressants provide improvement in moods, but they worsen anxiety. Benzodiazapines such as Klonapin and Xanax can be effective in reducing anxiety but are reported to have little effect on depression for this biotype. High-copper females are usually intolerant of birth control pills or hormone replacement therapy since these treatments increase copper levels in the blood.

A primary natural mechanism for removal of excess copper involves binding to metallothionein (MT) proteins in the liver, followed by excretion via the bile duct. The genetic expression (production) of MT proteins is dependent on zinc, and this trace metal is usually depleted in high-copper persons.

Increasing MT protein levels using supplements of zinc together with manganese, glutathione, vitamins B-6, C, and E, and other nutrients known to increase MT activity. This therapy must be introduced gradually to avoid sudden release of excess copper into blood that could cause a temporary worsening of depression and anxiety. Patients currently taking psychiatric medications should continue them during the initial two to three months of nutrient therapy. However, more than 85% of high-copper patients report that psychiatric medication can eventually be eliminated without the return of depression.

Elevated serum copper is exhibited by most women with a history of postpartum depression (PPD). Moreover, the classic symptoms of PPD are consistent with elevated norepinephrine and depleted dopamine that can result from copper overload.

  • Characterized by depressed mood, lack of energy, disruptions of sleep, high anxiety, reduced interest in previously enjoyable activities, and, in severe cases, suicidal and homicidal ideation and behavior. Most women experience mild depressive symptoms soon after childbirth, and 10-20% will experience a full-blown depressive episode. Normal pregnancies involve greatly increased levels of estrogens and copper in blood. During the nine months of a normal pregnancy, serum copper typically doubles from about 110 mcg/dl to about 220 mcg/dl. This additional copper enables rapid development of blood vessels (angiogenesis) needed for normal growth of the fetus. Normally, copper and estrogen levels begin to drop within 24 hours of delivery. It appears that PPD women have a genetic or acquired inability to eliminate excess copper.

Kathleen – 34 (Hypercupremia):

  • Symptoms of copper overload included history of childhood hyperactivity, ringing in the ears, skin sensitivity to cheap metals, inability to tan, and severe worsening of depression after hormone therapy.
  • Her serum copper level was 212 mcg/dl, compared to the normal range of 85-115 mcg/dl, and plasma zinc was out of range low at 65 mcg/dl. Initial treatment involved 25 mg/day of zinc, with the dose gradually increased to 75 mg/day.
  • Kathleen complained of heightened anxiety during this period. Her complete program included ample amounts of B-6 and PLP together with supplements of manganese, DMAE, and vitamins B-3, C, and E. At her 6-month follow-up evaluation, Kathleen’s metal levels had normalized and she reported that her depression was gone and that her marriage was solid again.

Carol – 31 (Hypercupremia):

  • Free of depression until she started birth control pills at age 16. Despite chronic depression, she excelled in college and had begun a successful career by age 24.
  • Depression had become very severe with persistent thoughts of killing herself by crashing her car into a concrete viaduct. She was too embarrassed to have counseling but tried Effexor, Paxil, and Zoloft in the recent past without improvement. She exhibited symptoms of copper overload including intolerance to chocolate, allergy to shellfish, extreme skin sensitivity, and occasional rages.
  • Carol’s lab results revealed elevated serum copper and depressed plasma zinc, and she was diagnosed with a metal metabolism disorder. Her therapy consisted of nutrients known to promote MT protein activity including zinc, manganese, selenium, DMAE, glutathione, 15 protein constituents of MT, and vitamins B-6, C, E, and PLP.
  • Susan called several times during the first two weeks of nutrient therapy concerned that her depression appeared to be worsening. However, she noticed clear improvement during month two, and after six months she stated that she was depression free for the first time in eight years.

Pyroluric Depression

Approximately 15% of the 2,800 persons in our depression database exhibited elevated pyrroles as their dominant chemical imbalance. This is a stress disorder with onset of depression often triggered by severe emotional or physical trauma.

Most pyrolurics experience about 50% of the following symptoms and traits: severe mood swings, inability to cope with stress, rages, absence of dream recall, sunburn tendency and inability to tan, morning nausea, and sensitivity to bright lights and loud noises.

Many persons with severe pyrrole disorder have slender wrists, ankles, and neck, while having great amounts of fat at their midsection and upper thighs. Female pyrolurics may report disturbed menstrual periods or amenorrhea.

  • Persons with this depression biotype are prone to delayed puberty and significant growth after age 16. Other symptoms include great inner tension, reading disorders, and academic underachievement regardless of intelligence. They tend to be fearful and pessimistic persons and isolate themselves from others. Many persons with this biotype are diagnosed with rapid-cycling bipolar disorder because of extreme mood swings that may occur many times daily.

Persons with pyrrole disorder suffer from a double deficiency of zinc and vitamin B-6 that may be genetic in nature. This results in a tendency for low brain levels of serotonin, dopamine, and GABA, which is a recipe for depression and anxiety. Nutrient therapy for pyrrole disorder simply involves normalization of zinc and B-6 levels.

Pyrrole disorders indicate elevated oxidative stress: ample dosages of selenium, glutathione, vitamin C, vitamin E, and other antioxidants assist in treatment. Depressed persons with pyrrole disorder respond more quickly to nutrient therapy than the other depression biotypes. Clear improvement is usually noticed within a few days, with the therapy achieving full effect within four to six weeks.

Because of morning nausea, many persons with pyrrole disorder cannot tolerate nutrients until lunchtime. They tend to perform badly in morning and are at their best late at night.

Curt – 24 (Pyrrole):

  • He disliked academics and took a job with the railroad after graduation. He was famous for his temper and had several arrests for assault. Curt complained of chronic depression and suicidal ideation since the age of 16. He was muscular with Hollywood good looks and had a very engaging personality. He was interested in girls but seldom dated because of embarrassing erectile dysfunction.
  • He reported several symptoms consistent with pyrrole disorder, including internal tension, poor short-term memory, absence of dream recall, enjoyment of spicy foods, pale complexion, avoidance of breakfast, and sensitivity to sunlight.
  • Urine pyrroles that were 10 times above the normal level. His nutrient therapy involved powerful doses of vitamin B-6 and zinc along with augmenting nutrients aimed at lessening oxidative stress (selenium, manganese, vitamins C, and E).
  • After two weeks of nutrient therapy, Curt called to report that he felt “weird” and was concerned that the vitamins were changing his personality. He was experiencing internal calm for the first time in his life and was alarmed at the striking change. At a 3-month check-up visit, Curt reported his depression had disappeared along with his violent temper but that the erectile dysfunction problem remained.

Marianne – 32 (Pyrrole):

  • She reported a troubled childhood that included special education and treatment for depression and intermittent explosive disorder. Her depression and emotional outbursts continued despite treatment by three psychiatrists who prescribed more than a dozen psychiatric medications in an attempt to help her.
  • She exhibited several symptoms of pyrrole disorder, including abnormal menstrual cycles, inability to handle stress, wild mood swings, white spots on fingernails, and morning nausea. In addition, she wore dark sunglasses throughout daytime hours and stated that she had never experienced a dream. Her urine sample turned a reddish-purple mauve color during storage in the lab refrigerator, and her pyrrole level tested at 82 mcg/dl.
  • Marianne was diagnosed with severe pyrrole disorder and was treated with strong doses of vitamin B-6, PLP, and zinc in conjunction with augmenting nutrients aimed at reducing oxidative stress.
  • Marianne’s parents reported that she underwent a transformation over the next four months. They were especially pleased that she appeared much happier, and her emotional outbursts had ceased. Two years later, we learned that Marianne had a steady job and was living independently in an apartment.

Toxic Overload Depression

Approximately 5% of the 2,800 persons in their depression database exhibited toxic-metal poisoning as their primary chemical imbalance. Most of these cases involved overloads of lead, mercury, cadmium, or arsenic.

Common features of this depression biotype are the following:

  • Depression that arises suddenly during a period of relative calm and wellness
  • Abdominal pain and cramping
  • Increased irritability
  • Headaches and muscle weakness
  • Low energy
  • Failure to respond to counseling or psychiatric medications

Toxic metal overload can be difficult to diagnose due to low concentrations of toxic metals in blood. An example of metal toxicity that does not usually show up in a blood test applies to the case of mercury: after a very short number of days, elevated mercury will not be found in the blood, having moved to other body tissues such as fatty tissue. Since depression due to metal toxicity is relatively uncommon, a logical first step is to rule out the presence of undermethylation, folate deficiency, copper overload, pyrrole disorder, casein/gluten allergy, or a thyroid imbalance. A careful chemical analysis of toxic metals in scalp hair can serve as a screen, recognizing the possibility of a false positive resulting from external contamination.

Many doctors test for toxic metal overload by introducing a chelating chemical that drives toxins from the body and then measuring the increased amount of toxins being excreted in the stool and urine. Unfortunately, reliable reference ranges have not yet been established for these challenge tests.

Young children are especially sensitive to toxic metals since their blood-brain barriers are still immature, and the toxins can interfere with the development of brain cells and receptors.

Depression, irritability, abdominal discomfort, kidney damage, and liver damage are the primary results of serious metal poisoning for adults.

Toxic metals in the brain can cause:

  • weakening of the blood-brain barrier
  • altered neurotransmitter levels
  • destruction or demyelination of the myelin sheath
  • increased oxidative stress
  • destruction of glutathione and other protective proteins

Nutrient therapy for lead poisoning involves supplements of calcium, promotion of metallothionein synthesis, and generous supplementation of antioxidants. Lead is a bone seeker with about 95% of old lead stored within the skeletal structure. In the absence of therapies to remove lead, the half-life of lead in humans is estimated at 22 years. Nutrient therapy and chelation techniques can effectively remove lead from blood and soft tissues but cannot rapidly remove lead from bone.

John – 54 (Toxic Overload):

  • He reported that counseling and several antidepressants had absolutely no effect on his condition. He also complained of uncharacteristic anger, nausea, and abdominal cramping. John’s lab chemistries were unremarkable except for a blood lead level 80 times above the normal level. John said he had purchased an old house and had spent the past six months scraping paint from the interior walls. They concluded that he had poisoned himself with repeated exposure to lead-based paint.
  • Since his depression was severe, he was hospitalized for several days and received EDTA chelation. Within a week, John reported that his depression was completely gone and that he decided to sell his house.
  • They prescribed supplements of calcium, zinc, selenium, and vitamins C and E to protect against lead that would be slowly leaching from his bones.

The half-life of mercury in the periphery of the body (everything except the brain) is about 42 days. The half-life of mercury in the brain has been measured at 70 days. However, mercury half-lives may be much higher for persons with a genetic metal metabolism disorder or severe oxidative stress. Mercury has a remarkable affinity for glutathione and MT proteins, and nutrient therapy that increases amounts of these proteins can effectively remove mercury from the body. Chelation and other therapies have been under active development for removal of mercury from autistic children.

Cadmium is especially dangerous since it tends to accumulate at kidney tubules and cause permanent damage. Sources of cadmium include shellfish, shallow wells, fertilizers, metal welding, brazing, fireworks, artist’s paints, mining operations, and various industrial plants. Cadmium is present in cigarettes, and smoking one to two packs daily can double blood and tissue levels of the metal. Cadmium removal must be accomplished with caution to avoid kidney damage, and treatments that enhance MT proteins are safer than chelation therapies that divert the departing cadmium through the kidneys.

Arsenic overloads are relatively rare and difficult to diagnose. The symptoms include upper respiratory problems, anorexia, muscle weakness, and irritation of mucous membranes. A definitive test for arsenic poisoning is the presence of elevated levels in both urine and scalp hair. Unfortunately, reference ranges for these assays are poorly defined, and interpretation of the results involves a degree of speculation. The biological half-lives of arsenic compounds are brief, ranging from 10 to 30 hours. The principal sources of arsenic are seafoods, contaminated drinking water, and pesticides. It has also been found on treated wood and playground equipment and in poultry feed. Nutrient therapy involving calcium and enhancement of glutathione protein levels can hasten the exit of arsenic.

Huberman

Mood Disorders & Maintaining Mental Health (Protocol 1)

The pleasure system is directly associated with the pain system. When we pursue something that will bring us pleasure, we experience the release of dopamine in pursuit of something. Afterwards we have a tilt of pleasure/pain balance. We experience this pain as craving for more. If we remain in constant pursuit we will receive less dopamine each time, and eventually end up addicted. We should always be cautious of any pursuit that leads to a large release of dopamine.

Major Depression

Bipolar depression is characterized by manic highs followed by crashes. Major depression (unipolar) is not characterized with these extreme changes.

Major depression impacts 5% of the population. The number 4 cause of disability. The dissection tool for depression is language. This makes it challenging to diagnose.

Clinical depression is characterized by grief, sadness, low threshold to cry, anhedonia (sad or neutral), guilt, sometimes negative delusional thinking, and confabulation.

“Anti-Self” Confabulation

They can make up elaborate stories without intent – self-deprecating stories that make them seem sick or not well even if they are actually getting better.

Autonomic (Vegetative) Symptoms of Depression

Symptoms that occur without thinking (autonomic). Constantly being exhausted and worn out. Something is off. Early waking and not being able to fall back asleep even if exhausted.

Usually early in the night SWS then REM later. It gets disrupted in depression. Affecting your emotions during the day. A signature of depression is the cortisol release in the later part of the day (9pm) instead of early.

Decreased appetite. Hormones must be impacted for these symptoms to be occurring.

Sad, guilty, exhausted, and often anxious.

Norepinephrine, Dopamine & Serotonin

Tricyclic antidepressants and MAOIs largely worked by increasing norepinephrine. They were found while trying to look for drugs that worked on blood pressure. Increasing the blood pressure is one of the side effects when trying to treat depression, as well as low libido, dry mouth, etc.

They then found pleasure and motivation pathways.

SSRIs (Prozac, Zoloft, etc.): Selective Serotonin Reuptake Inhibitors

Work by preventing serotonin from being cleaned up from the synapse, leaving more in the synapse for activation.

About a third of people that take them don’t get any benefits. There are also side effects. However, that have helped a lot of people. Relief doesn’t usually occur for a few weeks.

SSRIs might be able to trigger neurons in the dentate gyrus, which impacts memory. Also, possibly opening periods of critical plasticity.

Epinephrine/Motor Functions, Dopamine/Motivation & Craving, Serotonin/Emotions

Epinephrine deficit is thought to relate to psychomotor deficits (lethargy).

Lack of dopamine leading to anhedonia.

Serotonin deficit, the feeling of guilt or grief.

Unfortunately, we can’t just offer the specific drugs to deal with these symptoms. It doesn’t work that easily.

Physical & Emotional Pain are Linked: Substance P

Pain relievers seem to help with some emotional pain. However, opioids are highly addictive and prone to abuse.

Substance P is manufactured by our neurons that underlie our sensation of pain. A lot of people with depression are hypersensitive to pain.

Hormones & Depression: Thyroid & Cortisol

20% of people with depression have low thyroid hormone (hypo-thyroidal), leading to low energy, metabolism, and lethargy. Sometimes depression symptoms may be a thyroid problem.

Childbirth can give post-partum depression. So are post-menopausal women. More stress is correlated with higher rates of depression. 4-5 bouts of high stress events seem to be correlated higher with depressed states. The cortisol system can affect the hormonal system over time and suddenly the person becomes depressed months later.

Genetic Susceptibility to Depression: Impact of Stress

5HTTLPR is a gene that is a serotonin transporter gene, regulating how much is in the brain. Greatly shifting susceptibility to depression.

With each bout of stress, the probability of major depression goes up. With this gene, is goes up much faster.

Understanding Biological Mechanism Is Key: Recipes versus Skills

Learning about mechanisms is the difference between following a recipe and knowing why you do what it is telling you. So, you can be more flexible and adjust when necessary. If you just follow a recipe you have to stick to all the rules and ingredients.

Tools for Dealing with Depression: Logic & Implementation (Protocol 2)

If aspects are related to norepinephrine, taking a cold shower may relieve certain aspects. Exercise can increase epinephrine, also dopamine and probably serotonin if you enjoy it. Exercise is a protective mechanism of depression too.

If you are far along in your depressive state, you may not have the energy to get up and do things.

The reward circuits are present in everyone but they can’t access those circuits like others can at that time.

Brain Inflammation & Mental State: Cytokines, Prostaglandins, etc.

Many forms of major depression relate to excessive inflammation gone unchecked. Inflammatory cytokines, TNF-alpha, CRP, etc., inflame our brain and glial cells become disrupted. E2 prostaglandins can cross the BBB.

Protocol 3: Essential Fatty Acids (Omega-3, EPAs: Eicosapentaenoic Acid) *

Increase our intake of EFAs. The relief from taking EFAs (particularly 1g of EPA) matches SSRIs. People who took 400mg to 4000mg got benefits. For every gram ingested is about a 9% increase in CV health.

How EPAs Help Offset Depression: Serotonin Synthesis, Kynurenine, Quinolinic Acid

Inflammatory cytokines inhibit the release of NE, DA, and serotonin or the synthesis.

Tryptophan arrives through the diet and leads to an increase in heavy carbohydrate foods in depressed people. If there is excessive inflammation, the tryptophan is converted, which involves indolamine, into kynurenine. This acts as a neurotoxin by converting into quinolinic acid, which is pro-depressive. Ingestion of EPAs can cause more of the tryptophan to go down the serotonergic pathway.

Protocol 4: How Exercise Offsets Depression

Exercise tends to sequester, or shuttle kynurenine into the muscle so that it isn’t converted into that toxic molecule. Eat EFAs to limit inflammation and exercise to augment the conversion.

The mechanisms all seem to converge on serotonin.

https://www.tandfonline.com/doi/abs/10.1080/07315724.2009.10719785

Protocol 5: Creatine Monohydrate, Forebrain Function & NMDA receptors*

Can draw more water into muscles and increase power output. There is also a phosphocreatine system in the brain, particularly the forebrain is known to be involved in the regulation of mood and reward pathways, as well as improve symptoms of depression.

Creatine monohydrate in particular. It has been shown to augment or enhance the response to a SSRI in women with MDD.

Some studies show a relationship between the phosphocreatine system and the NMDA receptors. Which is the receptor that gate neuroplasticity. It is activated when circuits are going to change. This is especially important in depressed people who require a change in affect and mood.

Creatine has been shown to increase mania in people who are already manic though.

https://www.mdpi.com/2218-273X/9/9/406

Protocol 6*: Ketamine, PCP (*Prescription-Only), & NMDA-Receptor Function

They create dissociative anesthetic states. A particular layer of cortex (neocortex/layer 5), went into a 1-3Hz rhythm with ketamine or PCP. The dissociative state seems to allow them to disconnect from their issues so they don’t feel as overridden and burdened by their emotions. Distancing them from their grief and guilt. Needs a lot more research first though. They block the NMDA receptor.

Layer 5 of the cortex may be important for rewiring the brain in certain ways that alleviate symptoms of depression.

The spine formation on neurons is synonymous with neuroplasticity of the neuron and increase surface area to connect to other neurons. Ketamine can change the spines on the neurons.

Protocol 7*: Psychedelics (*In Clinical Trials) for Major Depression: Psilocybin*

Psilocybin has the capacity to rewire circuits and alleviate depression. It acts on the serotonin 5H2A receptor.

1 or 2 rounds of psilocybin depending on body weight, randomized. Significant improvement of mood in 70% of MDD people. The people had different experiences but it did not seem to matter to the actual effects on their depression symptoms. The activation of the serotonin receptors is offering an experience where the lateral connections are able to activate much more broadly. Somehow rewiring associations between events/experiences to relieve themselves from these narratives. Immersion here vs. the dissociation in ketamine.

Micro-dosing effects don’t seem anywhere near as powerful.

MDMA seems to have all its research in trauma.

https://jamanetwork.com/journals/jamapsychiatry/fullarticle/2772630

Protocol 8: Ketogenic Diet, GABA (Gamma-Aminobutyric Acid)

Ingestion of carbohydrates is the self-medicating reflective behavior. The keto diet seems to maintain euthymia – the state of equilibrium between manic and low in bipolar depression. It can provide some relief for MDD symptoms. It may even improve the effect of the antidepressant drugs in those that respond to them.

In epilepsy, the keto diet can greatly reduce epileptic seizures via GABA transmission. GABA can reduce neuronal firing. Alcohol also increases GABA but there is a rebound excitability once you stop drinking, terrible for epilepsy. Increasing ketone metabolism modulates GABA so that it is more active and to balance the glutamate:GABA ratio.

Benzos also increase GABA.

Fermented foods for the microbiome are another good way of supporting your body’s ability to manage symptoms.

Whole body hyperthermia: https://www.tandfonline.com/doi/full/10.1080/02656736.2021.1991010

https://www.foundmyfitness.com/topics/depression

Increased physical activity: https://www.foundmyfitness.com/news/stories/bdkynh

Exercise reducing depression: https://www.inverse.com/mind-body/exercise-depression-treatment-study

Depression and suicide linked to air pollution: https://www.theguardian.com/environment/2019/dec/18/depression-and-suicide-linked-to-air-pollution-in-new-global-study

Yoga, GABA, and depression: https://www.bumc.bu.edu/busm/2020/02/03/researchers-identify-link-between-decreased-depressive-symptoms-yoga-and-the-neurotransmitter-gaba/

Treating depression with omega-3: https://www.sciencedaily.com/releases/2010/06/100621111238.htm

Phobias

Fatigue

Eating too often lowers orexin, which lowers concentration and energy. It is stimulated by low glucose. Glucagon release also increases orexin, while carbohydrate intake suppresses it. Protein stimulates the orexin system. Narcolepsy has a connection associated with type 2 diabetes and obesity. Obesity is associated with low levels of orexin. Carbs restricted to dinner may help to improve alertness and increase sleep quality at night. Those who fast and struggle with energy may be due to low electrolytes. Replace sodium, limit caffeine. 

Bipolar Disorder

Eating Disorders

Huberman

Defining & Diagnosing Eating Disorders

Diagnoses should really be carried out by an expert trained in them. So, if you think you have some sort of condition, go see a qualified professional.

Anorexia Nervosa (Overview & Myths)

Most prevalent and most dangerous. The probability of death, if unaddressed is very high. It is a failure to eat enough to maintain a healthy weight. Low muscle mass, low fat mass, low libido, low heart rate, low blood pressure, hair growth (an attempt to insulate the body), loss of menstruation.

Rates of anorexia are not going up (recorded from the 1600s). So, it is hard to correlate it with the recent media obsession of unrealistic body types.

Bulimia (Overview & Myths)

Binge eating or overeating. Also very common, more in young women than men. Might be increasing. Not necessarily associated with anorexia, but can be comorbid. Clear biological underpinnings.

Binge Eating Disorders, EDNOS, OSFEDS, Pica

EDNOS – eating disorder not otherwise specified.

OSFED – other specified feeding or eating disorder

Pica – eating inedible objects like paint, dirt, rocks, etc.

What is Hunger? What is Satiety?

Mechanical information and chemical information are going to the brain as feedback from the body. When the stomach is full, it sends this mechanical feedback to let it know to stop eating. There are also neurons that detect chemical information like glucose, fatty acids, and aminos.

Neuronal & Hormonal “Accelerators & Brakes” on Eating

Your hypothalamus has POMC neurons that act like a brake on appetite. These are activated by sunlight too, which is why we tend to not need to eat as much during summer months.

The AgRP neurons are the ones that stimulate feeding and create an anxiety/excitement about food. A ramping up of energy. Animals and humans with overactivation of these neurons are anxious and will overeat and override mechanical and chemical signals to stop.

Fat, Leptin & Fertility & Metabolic Dysfunctions in Obesity

The more body fat we have, the more we secrete leptin, which goes to the brain to suppress appetite. It is suppressed in those with bulimia and obesity. When there is sufficient levels of body fat and leptin circulating, the hypothalamus and pituitary gland trigger the deployment of eggs in females and sperm in males. Injected leptin doesn’t seem to help anorexics or obese people.

There are also the signals from fatty acids, glucose, and amino acids.

Why We Overeat

From an evolutionary standpoint it makes sense that we should eat as much, as often, and as fast as we can. Every animal, including humans, has a hardwired circuit to determine how much food is available, how much we have now, and the possibility of food in the future. The POMC neurons in the arcuate nucleus start getting active when we see or think about food to drive hunger in a way that is responsive to what food looks like, smells like, prior history with that food, and social context (competition).

It is like bulimia and anorexia has lost top-down control and is correlated with impulsivity.

Homeostasis & Reward Systems/Decisions

There are things we know we should do and the things we actually do. In between those boxes are homeostatic processes (hot/cold, awake/sleep, desire/relaxation) that regulate the balances of your reward systems. Anorexia seems to be a disruption of these homeostatic and reward processes, such that decision making is disrupted. They don’t seem to be able to intervene between what they should do and actually do.

Anorexia

Anorexics have a switch that’s been flipped so that their decision making is actually really good, but their habits have been disrupted. They aren’t even consciously aware that they are making terrible/dangerous choices.

Found in all societies, even ones that are scarce. Some sort of reward mechanism that rewards them for not eating. It requires a hormonal disruption for classical diagnosis.

Typically starts around puberty during changes in brain circuitry in those that find food aversive. Symptoms of developing anorexia during puberty include: hypogonadism, amenorrhea, reduced insulin secretion, cosmically high levels of cholesterol.

The Cholesterol Paradox

Cholesterol is made from the liver in anorexics that consume very little food. Overshooting the mark since they won’t be used for sex steroid hormones.

Psychological vs. Biological/Genetic Factors in Anorexia

Possibly a child watching non-eating behavior of a mother may adopt these behaviors, or genetic influence, praise for eating control, etc. Hard to know. If one is rewarded enough, on top of genetic susceptibility, they may rewire the brain to favor this behavior.

Chemical Imbalances, Serotonergic Treatments

Serotonin increases the activity of neural circuits that promote satiety, enough food, warmth, social connection, etc. Drugs that improve serotonin levels have had some success. The goal is to increase their hunger though.

Altered Habits & Rewards in Anorexia: Hyperacuity for Fat Content

Anorexics, rather than being anxious about food, were hyperaware of the fat content of foods. Reflexively avoiding high calorie foods. The hallmark of a habit is it is reflexive.

Brain Areas for Reward Based Decision Making vs. Habits

Reward based decision making is controlled by the ventromedial prefrontal cortex. Duration path and outcomes type processes (DPOs) are for goal type behaviors. Very conscious process and reward based. Can be used for long decisions like planning a degree. All relies on the forebrain (PFC). Very metabolically demanding.

Reflexes do not rely on the PFC and don’t use as much energy.

The DLPFC is involved in decision making and evaluation of food selection. However, in anorexics, the dorsal lateral striatum was activated afterwards – habit based/reflexive avoidance of foods.

Habit-Reward Circuits Are Flipped in Anorexics: Reward for Deprivation

The reward systems have been attached to the execution of habits that are unhealthy for bodyweight and avoiding particular foods. They feel good (possibly dopamine) when they avoid certain foods.

The dorsal lateral striatum is involved in GO, NO-GO tasks. The GO, NO-GO circuitry is another aspect of behaviors to perform or suppress. The anorexic has restructured their system to favor non-caloric foods and the NO-GO high calorie foods.

Telling them that they are doing damage to themselves won’t work.

How Do You Break a Habit?

Teach the individual what is leading up to the habit and the internal state so they can learn to associate the interactions with the cues within their body (hyper-acuity of focus, quickening heart rate, etc.).

Weak central coherence is essentially an inability to see the forest through the trees (hyper-acuity). They are great at honing in on details.

They can’t seem to relax and enjoy the meal; they constantly monitor how much people are watching and are rewarded for certain food avoidance.

Family Based Models, Cognitive Behavioral Therapy

The entire family is made aware of their challenges. They stop condemning and start queuing good behaviors, as well as giving autonomy. Falls under CBT and can be combined. Relapse is about 50%. So far, the most effective treatment.

MDMA, Psilocybin, Clinical Trials, Ibogaine

Clinical trials are currently being done.

Seizure disorders have been found to happen with ibogaine treatment.

The anorexic needs a neurocircuit change where what was once rewarded is now punished and vice versa.

Knowledge of knowledge allows us to intervene. When we are tired, hungry, or intoxicated that ability to utilize that knowledge is impaired. Anorexics are known to constantly exercise.

Anabolic vs. Catabolic Exercise, Spontaneous Movements, NEAT

Helping anorexics to put on muscle weight can be a useful transition. Rewarding exercise for making one’s body strong, instead of focused on weight loss on a treadmill. NEAT is very high in people that fidget.

Distorted Self Image in Anorexia

Anorexics will often see themselves as overweight, regardless of the reality. They have a genuine distortion of their self-image. With better behavior, they start to also change their self-image.

Bulimia & Binge-Eating, “Cheat Days”, Thyroid Hormone

They ingest far more calories than they need. Often overriding mechanical signals. Once a month over a period of 2-3 months may qualify for bulimia. They are driven from the inside to ingest more than they need or even want to eat.

Vomiting and laxatives can cause serious damage to the esophagus, shame affecting mental health, digestive issues, etc.

Inhibitory Control, Impulsivity, Adderall, Wellbutrin

Lack of inhibitory control. Hyper-impulsive. Some are sexually promiscuous or eat wildly with a little alcohol.

Some drugs that increase serotonin or Adderall can help – DPOs become more active. Drugs that increase serotonin, sometimes dopamine and epinephrine too, can increase the adrenergic tone of the PFC.

Wellbutrin mainly increases dopamine and epinephrine levels for depression and obesity. Can be used.

Direct Brain Stimulation: Nucleus Accumbens

The nucleus accumbens is associated with dopamine release. Delta oscillations from the NA are associated with food reward. Making it hyper rewarding.

Many people who have bulimia are also obese, so they have even more reasons to seek help. Along with other conditions making life challenging.

Anorexia/Reward. vs Bulimia/Binging

Anorexia seems to be a disruption of habit and a coupling of unhealthy habits to the reward pathway.

Bulimia and binging and unhealthy gorging make them feel terrible and full of shame about their lack of control. The reward is set up before behavior, no impulse brake.

Borderline Personality Disorder

Insomnia

Refined carbs trigger insomnia: https://www.sciencedaily.com/releases/2019/12/191211171335.htm

Addiction

On Addiction (Hunter Gatherer)

Many things have a pathological version. Pathology is not the same as “downside”—senescence is a downside of early adaptive traits, but it is not pathological. In contrast, arrogance is pathological confidence.

Positive obsession has many words in English: passion, focus, drive. The primary manifestation of negative obsession, of pathological obsession, is addiction.

Our software is built to maximize our fitness, even if our conscious minds have other priorities. But our software has an increasingly difficult time telling signal from noise, because our map of what enhances fitness in the ancestral world does not prepare us well for the modern world.

Our intuitive sense of the fitness value of behaviors is thus often wrong in modernity. Our intuition had a greater chance of leading us to the right choice before the Industrial Revolution, before hyper-novelty was ubiquitous. Many of us are now effectively able to pull levers, like rats with access to amphetamine, and get a concentrated burst of euphoria that doesn’t just obscure the risk of that euphoria, but makes it ever less likely that we can turn away from it in the future. It’s another instantiation of the Sucker’s Folly: the reward obscures the cost.

“Reward” is not binary—it is not simply a positive or a negative. The valence and size of the reward depend, in part, on what the other possibilities are—the opportunity cost. The cost-benefit analysis is incomplete until you compare it to what else you could be spending the time on.

Boredom is effectively synonymous with the “opportunity cost” having gone to zero: if you believe there is nothing else enriching that you could spend your time on, then the calculation of whether or not to engage with a particular substance or action is skewed, particularly if that substance or action results in a feeling of enrichment, even a false one.

  • It is, of course, too simple to say that boredom causes addiction. There are many factors at play: the limiting nature of ancestral environments did not require self-regulation for most substances or behaviors; both trauma and psychological disorders disrupt decision-making processes; emotions are hijacked by addictive substances and behaviors that create a false incentive structure; and social pressures often drive calculations toward consumption.

Alcohol Abuse

  • Chronic alcohol abuse and protein deficiency also hurt vitamin A utilization.
  • Benfotiamine may be beneficial for the neuropathy of diabetes and alcoholism but its superiority over thiamin hydrochloride has not been clearly demonstrated. Thiamin pyrophosphate (thiamin diphosphate) is the active form of thiamin, and supplements of this form could plausibly overcome impairments in thiamin activation, which are known to occur in alcoholism.
  • Anorexics and alcoholics have poor intake, and alcohol impairs the absorption and utilization of riboflavin and niacin.

Huberman

Dopamine Fundamentals: Precursor to Adrenalin

The substrate of which adrenaline is made. The brain is where epinephrine is made. Epinephrine allows us to get into action. Dopamine was initially only seen as the building block for it.

The Reward Pathway: An Accelerator & A Brake

Important for your desire to get into action. The ventral tegmental area contains neurons that spit out dopamine on the nucleus accumbens. They form the core machinery of the reward pathway. The brake on dopamine is the prefrontal cortex, which stops us being purely pleasure seeking.

Motivation= Pleasure Plus Pain

When doing nothing, the reward pathway fires at a low level. If suddenly you get excited in an anticipatory way, release goes up 30-40 times. Wanting and craving a particular thing. Dopamine doesn’t care what you’re craving.

The Dopamine Staircase: Food, Sex, Nicotine, Cocaine, Amphetamine

Sex makes it go up by about 100%, nicotine increases very quickly by about 150% above baseline. Cocaine and amphetamines by about 1000%. Just thinking about food, sex, and drugs can make it go up by almost to the same degree as the drug. Enough to get them on the motivation track.

Social Media and Video Games

High update and novelty speeds release about as much dopamine as cocaine. Social media levels taper and yet we still get addicted.

Addiction & Dopamine: Progressively Diminishing Returns

Novelty, Sensation-Seeking & Anticipation

Some people have a heavy bias with the first attempt of addictive stuff. When you try something addictive you get a dopamine release and a mirror experience that effectively causes pain. A piece of chocolate is a good way to experience it. Pain is felt without it so you continue to eat it.

Craving: Part Pain, Part Pleasure & Pain Always Prevails

Each time you engage in addictive behavior, the joy goes down. The amount of pain and craving increases though.

Desire Scales with Pain: The Yearning Function

Desire is about pursuing pleasure and also the desire to pursue something that reduces the amount of pain.

Even if yearning is psychological, it will feel as physical pain.

Caffeine May Protect Dopamine Neurons, Methamphetamine Kills Them

Can increase dopamine by 30% and may have a protective effect on neurons. Low levels of caffeine anyway.

Nicotine: Dopamine, Possible Neuroprotection, Prolactin Increase

Nicotine can increase prolactin.

Gambling, Intermittent Reinforcement, & Persistent Goal Seeking (Bad and Good)

The next time could be the one that changes everything. Intermittent reinforcement strategy is the most powerful dopamine reward scheduling.

Intermittent Halting of Celebration; Enjoy Your Wins, But Not All of Them

To remain on a path to a goal while still being rewarded by dopamine is to remove reward responses intermittently. Reduce the impact of the reward. Don’t celebrate too intensely to keep dopamine in check. Celebrate your wins but not all of them.

You can make somebody else responsible for designating the reward at their discretion.

Huberman and Anna Lembke

Dopamine, Happiness & Impulsivity

Dopamine is released when food is sensed in the environment. We are always releasing dopamine at a tonic rate. Going below the baseline may result in a perception of pain.

People who are depressed may have lower tonic baseline levels. When constantly exposed to high amounts of dopamine we can possibly change that baseline.

People who are more impulsive are more vulnerable to addiction.

What we now consider mental illness are actually traits that may have been advantageous in a different ecosystem. We are currently living in an extremely sensory rich environment and being bombarded with opportunities and need to keep checking ourselves.

What Is Pleasure?

Seeking pleasure is often a way to escape pain. There is also the desire for pleasure for the hedonic experience itself.

Addiction, Boredom & Passion for Life

Life is boring because all our survival needs are met, even if we are poor. We also have excessive leisure time. Meaning we all need to make stuff up to do. Some people, if they don’t have friction, they are unhappy. A sense of restlessness, not knowing what is wrong. Their brain is not suited for this world.

Pain-Pleasure Balance Controls Addiction

Pleasure and pain are co-located. They tip back and forward but want to be balanced. Pushing in any one way will cause a deficit. Too much pleasure will create a longing and desperation for more.

Repetitive social media, food, sex, etc., dopamine release, pain moves higher on the scale, making pleasure less rich.

Dopamine Deficits, Anhedonia

The comedown after indulging. If you don’t wait for your pleasure-pain balance to come back to normal, you will create a higher dopamine threshold.

Are All Addictions the Same?

Once you’ve been addicted to a substance or behavior you will be more likely to be addicted to others. Even workaholism is heavily rewarded and addictive.

Addiction is a progressive narrowing of the things you enjoy. Enlightenment is a progressive expansion of the things that bring you pleasure.

Boredom & Anxiety Lead to Creativity

People who get addicted and go into recovery have a hard-earned wisdom.

Some kind of flexibility/resilience in our dopamine balance. We should learn to live in a world that can be boring. Boredom is highly anxiety provoking because it is so rare now. When you allow yourself to be bored it can feel like there is nothing left to do. Allowing space for creativity. Not being distracted anymore.

Finding Your Passion Starts with Boredom & Action Steps

Stop looking for your passion and instead, look around at what needs to be done. Even something as simple as throwing out the rubbish. When you are no longer searching for the perfect thing, you can find humility and peace. Not to mention actually finding some way of being productive.

In the act of looking in one’s immediate environment and acting on it we cultivate the relationship to the circuits in the brain about action and reward spanning from small things to larger ones in a functional way.

People who wait for some sort of passion to pull them out of the video game world are unintentionally feeding their addiction and failure to find purpose. Abstain from video games, reset your reward pathways, start with a level balance, and try something. Things will suddenly start getting more interesting.

A sense of duty to do the immediate things can lead to incredible productivity. SEAL team members constantly scan the environment for things that need to be done. Essentially conquering their environment. They are also very competitive.

Our brain is wired for the 24-hour period. By living in the future, you become more anxious. Just work on a day at a time by being awake and alert. Drugs and video games take you away from your immediate environment and your authenticity.

How to Break an Addiction

In order to break an addictive pattern, you need at least 30 days of zero interaction with that substance/person. By depriving ourselves from these high dopamine rewards we allow the pathways to recover.

The first 10 days will be miserable. Pain will be ramped up, you’ll feel depressed and angry, social interaction will be horrible, etc. You need to take away access to the addiction. After two weeks there is a light at the end of the tunnel. “Let’s try this experiment.”

Relapse, Craving & Triggers

There are people who will die of their disease/addictions and it can be reasonable to think of it as a brain disease. For some people, they may still have an imbalance after 6 months to a year, as that balance has lost its resilience and ability to restore homeostasis.

Imagine you has an itch on your body and you are trying not to scratch it. As soon as your stop thinking about it, you reflexively scratch it.

Sometimes the dopamine associated with a win for some recovering addicts can trigger reuse. The dopamine levels may also drop below baselines and then drive for the drug/behavior to bump it back up. Good things and bad things can be a trigger. We need to remove the hypervigilant state for the risk to go down. While keeping in mind that the threat is always there so not to get complacent.

Can People Get Addicted To “Sobriety”?

Addicts seem to always want to talk about their recovery a lot. These people seem to want the big highs and lows still. Recovery meetings are always about extreme feelings. The reason AA is like a cult is why it works. It is the intensity of intimacy.

Are We All Wired for Addiction?

Some people are always seeking intense experiences, like holidays, too. As if going to these places will scratch some sort of itch.

We are all wired for addiction in some way or another. Some people are just addicted to things that are really socially rewarding, like working.

Recovered Addicts Are Heroes

The courage and discipline to recover from addiction is amazing. Especially in a world where we are constantly invited and tempted to do things. They also appear very wise.

Lying, Truth Telling, Guilt & Shame

Addicts often get in the habit of lying, not just about their usage but also small things. Truth telling is important. When we tell the truth we strengthen our PFC circuits and their connection to the limbic and reward brain. In addiction, these areas are essentially disconnected. The most intimate connections create dopamine and truth telling builds these connections.

Of the 12 steps of AA, one is making amends. Apologizing in which the ways we lied and harmed others. We need to experience an appropriate amount of shame.

Clinical Applications of: Ibogaine, Ayahuasca, Psilocybin & MDMA

Studies showing alcohol addicts taking certain psychedelics, on top of psychoanalysis, and therapy. Good support system while getting them out of their own heads. Gives them another lens to view their own lives. Some get worse, some get better. Trauma is another potential issue it can help.

A lot of people are now using these drugs by themselves as a form of spiritual adventure. Taking their mental health into their own hands. If people are going to attempt this there should be a controlled setting. The context might even be more important than the drug itself.

Social Media Addiction

It really is a drug and is engineered to be so. We need to be more thoughtful about how we use it. We can use it as a tool to connect but not abuse it.

Young people are basically cybernetically enhanced. So, regulation is the best we can do at this point.

Many pregnant mothers won’t put their phones down while giving birth now. A mature organism, mature in years, that can’t control its behavior is a baby. We need to be more intentional and set up barriers against distracting ourselves with these addictive technology using behaviors.

You are either consuming or creating.

Narcissism

Healthy narcissism – invest personal energy into things we care about. However, we are living in a narcissistic culture that has no shame in being so. Fueled by social media. Contributes to a lot of personal shame. We should be doing more together instead of finding ways to separate ourselves with achievement. We put a tremendous amount of pressure on ourselves. You’ll never win.

Goal Seeking, Success & Surprise

The prize that we aren’t trying to get seems to feel the best. Accumulating success without the desire for it is very process oriented. Working on the day and making things better. Being authentic and paying attention. What can I do today that can be of service?

Reciprocity

Align your compulsion with something good to support others.

There’s a general sense that if we give something to someone, we lose something.

To be researched

  • Gabor Mate: We have to attach to others to survive. Endorphins facilitate attachment. If there is stress and trauma in childhood, the endorphin systems don’t develop. Heroin and opiates create an immense feeling of comfort (attachment) in those who have been deprived. Authenticity (being connected to ourselves) is another human trait that is essential for survival. However, when authenticity threatens your attachment, the authenticity is repressed, e.g., a child suppressing their anger in order to hold on to the love and attachment from their parent. Resulting in a life of repressed authenticity/intuition (gut feelings). Healing requires a reconnection to the authentic self. Conflict often occurs in modern society when the need to conform places too much pressure on them. Trauma is the experience inside the person (disconnection from emotions/body, negative view of self and life, difficulty being in the present moment) and experiences that happen are traumatic. Addiction is not the problem; it is an attempt to deal with trauma. Instead of constantly revisiting the trauma in counselling, your time would be better spent reestablishing authenticity. Recovery is finding and reconnecting with your authenticity and self.    
  • Ketamine disrupts memories to help alcohol addicts recover: https://www.science.org/content/article/ketamine-disrupts-memories-help-heavy-drinkers-cut-back
  • The addict tends to have either more trauma or less support with their trauma compared to somebody else. The act of seeking out drugs is the “temporary state” to overcome an unbearable state. The addict doesn’t want to be addicted; they just want momentary inner peace. An external regulation rather than an experiential rehabilitation like while undergoing psychedelic therapy (facilitates change/growth).
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