Bartonella henselae. The bacteria behind cat scratch fever. 15 to 40% of cats carry it depending on age and flea exposure. Most doctors think the infection is mild and self-limiting. In some people it isn't.

It's an intracellular pathogen. Hides inside red blood cells and the endothelial cells lining your blood vessels, including the ones in your brain. Your immune system can't see it properly. It sits there causing chronic neuroinflammation for months or years.

Edward Breitschwerdt's lab at NC State has been documenting this for over a decade.

The research:

A 2019 case study: a boy developed sudden psychosis and seizures from confirmed Bartonella in his blood. Treated with antibiotics. Resolved.

A 2024 review from his lab called Neurobartonelloses: emerging from obscurity catalogued the full neurological damage - encephalitis, peripheral neuropathy, cerebral vasculitis, psychiatric symptoms including psychosis.

A 2024 study from Columbia and NC State tested 116 people. Patients with psychotic disorders were three times more likely to have Bartonella DNA in their blood than healthy controls (43% vs 14%, p=0.021).

A 2021 pilot study at UNC and NC State found the same thing. 65% of schizophrenia patients had Bartonella DNA, 8% of controls.

Two independent research groups. Two separate patient populations. Same result.

Why testing misses it:

Standard testing is an IFA antibody test. But Bartonella hides inside cells and your immune system may never mount a detectable antibody response. The Columbia study proved this directly — the antibody test could not distinguish patients with psychosis from healthy controls. The PCR could. Same blood, same patients, different test, different answer.

A negative IFA does not rule out Bartonella. It rules out a detectable antibody response. Those aren't the same thing.

Better tests: enrichment PCR or droplet digital PCR (ddPCR). Most doctors have never heard of either. You have to ask.

The symptom pattern:

• Brain fog that started suddenly, not lifelong
• Rage or irritability that doesn't fit your personality
• Anxiety or panic that SSRIs don't touch
• Insomnia the wired kind, not the tired kind
• Unexplained foot pain (endothelial inflammation and peripheral neuropathy)
• Linear raised marks on shins or thighs (look at your legs)
• Headaches that track the same timeline

Any one of these means nothing. Four or more with cat or flea exposure warrants testing.

The antibiotic clue nobody talks about:

If you've ever taken antibiotics for something unrelated dental infection, UTI, sinus infection and your brain fog temporarily improved, that's meaningful. Random antibiotics can partially suppress Bartonella. Most patients and doctors read this as evidence that the dental issue was the problem. It can also be evidence of a bacterial cause hiding underneath.

Treatment:

Chronic Bartonella requires targeted antibiotics for weeks, not days. The specific drugs and duration vary by species, severity, and individual response. This needs a doctor familiar with intracellular infection protocols. Herxheimer reactions (feeling worse before better) are common as bacteria die off.

What to ask your doctor:

• Enrichment PCR (BAPGM) or ddPCR testing, not just IFA
• Cat scratch history, not just "do you have pets"
• Whether any prior antibiotic course coincided with symptom improvement

Bartonella isn't responsible for every case of brain fog. It's worth checking when the symptom pattern fits and the fundamentals have already been addressed.

What about the cat

I'm not a vet. But here's what I learned when I went down this road.

Most cats that carry Bartonella show no symptoms at all. Your cat isn't sick. It's a carrier. You won't know by looking at it.

Kittens are higher risk than adult cats. They carry higher bacterial loads and they scratch more. Rescue kittens with fleas are the highest risk combination. That was my situation exactly.

Cats can be tested. A vet can run PCR on blood to check for Bartonella. But a negative doesn't mean they never had it. Cats can clear the bacteria on their own over time. A cat that infected you 6 months ago might test clean today.

The single most important thing you can do is flea control. Bartonella lives in flea feces. Fleas defecate on the cat. Feces gets under the claws. Cat scratches you. That's the transmission chain. Break it at the flea step and the rest doesn't happen.

Topical or oral flea preventative. Year round. Not just summer.

Beyond that. Keep claws trimmed. Don't let cats lick open wounds. If you get scratched wash it immediately and thoroughly. Don't play rough with kittens using your hands.

Don't get rid of your cat. That's not the message here. The message is keep the cat flea-free, handle scratches properly, and if you develop unexplained neuropsychiatric symptoms with the timeline and symptoms I described, tell your doctor you have cat exposure.

SOURCES

• Breitschwerdt EB et al. Bartonella henselae bloodstream infection in a boy with PANS. J Central Nervous System Disease. 2019. DOI: 10.1177/1179573519832014
• Lashnits E et al. Schizophrenia and Bartonella spp. Infection: A Pilot Case-Control Study. Vector-Borne and Zoonotic Diseases. 2021. PubMed: 33728987
• Bush JC, Robveille C, Maggi RG, Breitschwerdt EB. Neurobartonelloses: emerging from obscurity. 2024. PubMed: 39369199
• Delaney S et al. Bartonella species bacteremia in association with adult psychosis. Frontiers in Psychiatry. 2024. DOI: 10.3389/fpsyt.2024.1388442
• Breitschwerdt EB et al. One Health Zoonotic Vector Borne Infectious Disease Family Outbreak Investigation. Pathogens. 2025. DOI: 10.3390/pathogens14020110
• Breitschwerdt EB et al. Bartonella Associated Cutaneous Lesions in People with Neuropsychiatric Symptoms. Pathogens. 2020. DOI: 10.3390/pathogens9121023

Started with swapping bulbs in bedrooms and bathrooms. Did a few more in areas where time is spent in evening like dining room and den. The light is warm and I feel like my eyes hurt less. Anyone else have experience with this? Got thinking about the blue light after listening to Huberman podcast

I am looking for other peoples experiences with healing their brain after years of stimulant use, what worked, what didn't, what had the biggest impact? As the title suggests I have a very hard time feeling any form of happiness. My parents decided to put me on adderall when I was 5 years old, and I took it every day until I was around 21. When I stopped taking it I fell into a tremendous depression that left me sleeping every other day and never leaving the house. At time time I assumed this was related to a recent break up but as the years went on and I can't remember anything about that girl but her name, I am still dealing with day-in and day out misery. I just only ever feel scared or safe. Never optimistic, never happy.

Of course like most people in lieu of happiness I developed distractions like phone 24/7 gaming/sex/etc. I ever ended up having some pretty persistent issues with thrill seeking behavior/passively suicidal actions just to feel something. I also have tremendous anxiety all the time, even when I am sleeping. I understand that joy comes in a bunch of forms and includes socialization, meaning, safety, philosophy etc, but no matter what is happening in my life, or how any of those things feel, I just feeling fucking miserable.

An incomplete list of things I have tried for PTSD/depression and their benefits:

EMDR: I noticed no improvement

ECT: I did not notice any improvement but I do have an issue recalling about a 3 month period of my life

Becoming a therapist: I spent 5 years in school to become a therapist hoping that it would grant me the ancillary benefit of self help. No meaningful improvement in misery.

TMS: I think I noticed a small improvement, hard to say

SGB: I slept 16 hours a day for 2 weeks until the block wore off, no meaningful changes otherwise

Selank: I did not try the NA version but it seemed to make me zero % less miserable and slightly more anxious

Buspar: More anxious same misery

CBT: Helpful, good anxiety coping skills, not much else

Psychotherapy: Somewhat helpful, although more for processing

Yoga: Helpful, grounding. Not really any improvements in joy, optimism, etc

Exercise: Helpful for all counts. Some post work out euphoria, more optimism, better sleep.

Journaling: good for anxiety, zero effect on misery.

GB-115: I did not notice a meaningful reduction in my anxiety, no additional joy

So I am making this thread in the hopes that other people have had experience with dopamine and serotonin production after long periods of continued use of adderall especially in their developmental years, and especially in the hopes that someone has had success improving it.

tl;dr I literally never feel happy, only miserable, scared, or nothing, suspect adderall, what's the move.

Dopamine D2 receptor downregulation is the hallmark of addiction

https://preview.redd.it/bolwu22t1btg1.jpg?width=357&format=pjpg&auto=webp&s=ac094da7a0280ad62f720f93753d32762cbb1469

In the previous article in this series, I showed that the downregulation of dopamine D2 receptors is the hallmark of drug addiction. This view is widely shared by investigators of addiction (Trifilieff et al., 2013; Trifilieff and Martinez, 2014; Volkow and Morales, 2015). Note, this is a repost. Check them out here.

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All addictive drugs downregulate the D2 receptors. Non-addictive drugs tend to not downregulate D2 receptors.

D2 receptors in the medium spiny neurons (MSNs) of the indirect pathway, which connects the nucleus accumbens with the frontal cortex, are essential to maintain motivation, sustained effort and focused attention. Therefore, we could consider them the molecular foundation of mental energy.

Without enough D2 receptors, drug addicts live in a state of dissatisfaction and lack of motivation. They lack mental energy or, rather, all their mental energy is consumed by drug seeking.

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With this in mind, we can answer the questions of whether some behaviors, like sex, gaming or exercise, are 1) addictive and 2) decrease our mental energy. If so, they should downregulate the D2 receptors, like all addictive drugs do.

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The controversy: are behaviors addictive?

People who think that some behaviors are addictive often refer to a review paper from 2011 (Olsen, 2011). Table 1 of that paper summarizes the information in this regard and has been reproduced in Wikipedia. That table is a good source of references concerning the evidence that behaviors are addictive. In the columns, it lists five things that are supposed to induce addiction:

1. opiates,
2. psychostimulants (cocaine, amphetamines),
3. food high in fat and sugar,
4. sex,
5. exercise, enriched environment and sensory reinforcement.

https://pmc.ncbi.nlm.nih.gov/articles/PMC3139704/

Dopamine receptor - Wikipedia

Opiates and psychostimulants are stereotypical addictive drugs, so they are a good positive control for addiction.

It’s nice to have sex in its own separate category.

An enriched environment (see image) means that rats or mice are housed in cages containing toys, running wheels and other rats or mice (McCreary and Metz, 2016). It has been shown to increase the intelligence and lower the stress of the animals.

Sensory reinforcement means that the rats or mice are exposed to novel sensations, like new objects, food or smells.

Exercise, enriched environment and sensory reinforcement shouldn’t be lumped into a single category, since they may have different effects on the brain. However, they are unquestionably healthy, so they could serve as a control for things that should not be avoided. Still, the authors make it clear that they consider them too addictive behaviors.

Item 3, food high in fat and sugar, is the most tricky category. Some foods may be addictive because they produce spikes in insulin, a hormone that seems to have pronounced effects on the reward pathway (Davis et al., 2008).

Let’s now examine the different items on the rows of that table, which are proposed as markers of addiction. I exclude items that do not apply to sex and exercise / environmental enrichment / sensory reinforcement because they are not relevant to this discussion. I also exclude things that have opposite or inconsistent effects between opioids and psychostimulants, since they are not good markers of addiction.

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Downregulation of D2 receptors is in the 8^(th) row of the table.

As I stated before, opioids and psychostimulants downregulate them. So does food rich in fat and sugar. However, exercise / enriched environment / sensory reinforcement upregulate the D2 receptors, that is, they do exactly the opposite of addictive drugs. The entry for sex in empty.

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Cross-sensitization with psychostimulants, psychostimulant self-administration, and reinstatement of drug-seeking behavior are listed as markers of addiction in three other rows. Here again, exercise / enriched environment / sensory reinforcement have effects opposite of those of psychostimulants and opioids. This means that these behaviors decrease the interest in addictive drugs, that is, that they have anti-addictive properties. This is hardly compatible with the idea that these behaviors are addictive.

CREB phosphorylation decreases and delta**-FosB** increases in the nucleus accumbens head two other rows. They are affected similarly by addictive drugs and exercise / enriched environment / sensory reinforcement. However, these are general markers of neuronal activation. It makes sense that these three things activate neurons in the nucleus accumbens, because they activate the reward pathway. Exercise requires motivation. Sensory stimulation and a rich environment prod the animal into action.

In summary, exercise / enriched environment / sensory reinforcement have opposite effects from drugs on D2 receptors and drug seeking behaviors. This shows that these behaviors are not addictive, and even have anti-addictive properties.

A study examined social media “addiction” (Fournier et al., 2023) as defined by six components: salience, tolerance, mood modification, relapse, withdrawal and conflict. It found that these six components are not consistent with each other and are not associated with mental problems.

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Exercise

Some scientists consider exercise addictive (Olsen, 2011; Dinardi et al., 2021).

However, exercise has been known since the 80s to increase D2 receptors in the rodent striatum (MacRae et al., 1987; Bauer et al., 2020). In rats, High Intensity Interval Training (HIIT) increased D2 receptors, but not D1 receptors, in the shell of the nucleus accumbens (Tyler et al., 2023).

In humans, the results are less clear. In two patients with early Parkinson’s disease, treadmill training for 8 weeks increased D2 receptors, measured with [18F]fallypride PET imaging (Fisher et al., 2013). Another study in older subjects using PET with the D2/D3 receptor ligand [11C]raclopride (Jonasson et al., 2019) found that aerobic exercise did not increase D2 receptors. A study of 19 methamphetamine users with [18F]fallypride PET imaging found that exercise for 8 weeks increased striatal D2 receptors in the exercise group but not the control group (Robertson et al., 2016). This shows that exercise can be used to reverse the downregulation of D2 receptors produced by drug addiction.

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Gambling

Pathological gambling is the stereotypical compulsive behavior, the only behavior classified as addictive in the DMS-5 (Clark et al., 2019).

However, gambling did not change the amount of D2 or D3 receptors in the striatum or the substantia nigra (Boileau et al., 2013). In this human study, positron emission tomography (PET) imaging was used to measure the binding of an agonist of D3 receptors (PHNO) and an agonist of both D2 and D3 receptors (raclopride). No differences were found between 13 pathological gamblers and 12 control subjects.

A review of human studies (Clark et al., 2019) found no changes in D2 receptors in gamblers. In addition, MRI imaging found only small changes in gray and white matter in gamblers, while these changes are major in drug addicts. Functional MRI found some changes in the ventral striatum and the medial prefrontal cortex, but the direction of these changes was not consistent between studies.

Therefore, the neurophysiological profile of gambling is completely different from drug addiction.

D2 Variant involved in addiction

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The D2A1 variant of the human D2 receptor is involved in addiction

The human D2 receptor gene has several variants, which produce D2 receptor proteins with different functions. In particular, the Taq A1 variant (D2A1) is commonly found in drug addicts and alcoholics (Comings and Blum, 2000). It has been proposed that the reason for this is that individuals with this variant have an abnormal reward pathway, something that has been called reward deficiency syndrome (Blum et al., 1996; Comings and Blum, 2000). The D2A1 variant decreases the amount of D2 receptors and produces less cognitive flexibility (Fagundo et al., 2014).

Pathological gambling is also associated with the D2A1 variant of the D2 receptor. In a genetic study (Comings et al., 1996), 50.9% of the subjects with gambling disorder carried the D2A1 variant, compared with 25.9% of controls. The severity of the gambling disorder correlated with the expression of the D2A1 variant.

This supports the idea that having less D2 receptors causes compulsive behaviors. While addictive drugs downregulate the D2 receptors, in gambling the decrease in the D2 receptors is not due to the behavior itself, but to genetic causes.

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Does sex downregulate D2 receptors?

With all this in mind, we can address the questions of whether sex is addictive or causes a decrease in mental energy.

Unfortunately, I could not find any studies on the effect of sex on D2 receptors in the nucleus accumbens. One study in rats (Nutsch et al., 2016) found that sexual experience increased the number of neurons with D2 receptors in the medial preoptic area of the hypothalamus, a brain region in which dopamine and D2 receptors trigger copulation (Melis and Argiolas, 1995; Giuliano and Allard, 2001; Nutsch et al., 2016). It is possible that sex also upregulates D2 receptors in the nucleus accumbens.

In fact, sex has much in common with exercise, enriched environment (which includes social interactions) and sensory stimulation, activities that upregulate D2 receptors in the nucleus accumbens. Even gambling, the model “addictive” behavior, does not downregulate D2 receptors in the nucleus accumbens.

Therefore, we could infer that sex either has no effect or upregulates D2 receptors in the reward pathway. If so, sex should not be addictive or decrease the mental energy mediated by the reward pathway.

The data shown in the graph is not taken from an actual experiment, however, out of the data from the literature an approximate extrapolation and graphic depiction is made. The rectangles are the possible approximate concentrations of the neurotransmitters; they are merely assumptions to visualize the alterations of neurotransmitters during the sexual response cycle. https://www.researchgate.net/figure/The-release-of-various-neurotransmitters-during-the-phases-of-male-and-female-sexual_fig2_333616586

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Effects of dopamine on sex

Dopamine, acting on D2 and D4 receptors, has stimulatory effects on all phases of sexual activity: arousal, erection and copulation (Mas et al., 1990; Komisaruk et al., 2006; Melis et al., 2022). In men, the non-selective agonist of D1 and D2 receptors apomorphine has been used to treat erectile dysfunction (Giuliano and Allard, 2001). In female rats, dopamine facilitates sexual arousal and orgasm (Uitti et al., 1989; Shen and Sata, 1990).

However, these effects of dopamine on sex are primarily mediated by hypothalamic neuronal pathways, the incertohypothalamic, the tuberoinfundibular and the hypothalamospinal systems (Melis et al., 2022).

Although dopamine is released in the nucleus accumbens during sex (Mas et al., 1990), the importance of this for sexual behavior is considered marginal (Paredes and Agmo, 2004). Let’s keep in mind that motivation for any behavior involves dopamine release in the reward pathway. Mice with a mutation that makes them unable to release dopamine in the nucleus accumbens lack motivation to do anything at all, including drinking and eating (Wise and Jordan, 2021).

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Why is sex considered addictive?

Then, why do some scientists consider sex addictive? The evidence provided by Olsen (Olsen, 2011) is quite flimsy. He does not report any effect of sex on D2 receptors, psychostimulant self-administration and reinstatement of drug-seeking behavior. The main evidence he provides is the following.

Sex cross-sensitizes with psychostimulants, unlike exercise / enriched environment / sensory reinforcement. This means that rats addicted to cocaine have more sex. Conversely, rats that have more sex like cocaine. However, this doesn’t mean that the rats are addicted to sex. It could simply mean that once a rat is used to seeking a reward, it tends to do it more, no matter if the reward is sex or cocaine. Seeking a reward is not the same as being addicted to it.

https://preview.redd.it/mkmct8vc4btg1.png?width=500&format=png&auto=webp&s=4e2e29cf4df35d7ba891e64f6272af91de29b03a

Conditioned place preference is an experiment in which a rat gets an injection of a drug in one of two chambers. If the rat wants the drug, it will go back to the chamber where it was given the drug. If the rat doesn’t like the drug, it will avoid that chamber. A rat habituated to having sex chooses the same chamber where it has been given cocaine. Olsen takes this as an indication that sex is addictive, but this argument doesn’t hold to close scrutiny. Rats exposed to a rich environment also choose the chamber where they are given cocaine. However, not the rats habituated to exercise or to sugary food. Therefore, conditioned place preference is not a consistent indicator of addiction.

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The L-DOPA paradox

As I explained in a previous article, L-DOPA is a precursor of dopamine that is given to Parkinson’s patients to alleviate their symptoms. Since L-DOPA bypasses the regulation of dopamine synthesis by the enzyme tyrosine hydroxylase, it leads to a dramatic increase of dopamine in its synapses (Sulzer et al., 2016). Therefore, there is a greater release of dopamine.

The L-DOPA paradox is that, like all addictive drugs, L-DOPA produces an increase of dopamine in the nucleus accumbens, but it is not addictive. What L-DOPA does, in some of the patients taking it, is increase compulsive behaviors, mostly hypersexuality, but also gambling, overeating and shopping (Potenza et al., 2007; Ceravolo et al., 2010).

One possible explanation for this paradox is that, in patients who take L-DOPA, dopamine is still released in short spikes by natural stimuli, while addictive drugs produce long increases in dopamine. It could be that what leads to addiction is the duration of the dopamine increase, and not its magnitude. This is consistent with the idea that D2 receptor downregulation is what causes addiction. A prolonged increase in dopamine would lead to the repeated internalization of the D2 receptors, causing their degradation. In contrast, the brief spike in dopamine produced by natural stimuli internalizes the D2 receptor just once, no matter how high the spike is, and this does not downregulate the D2 receptors.

This supports the idea that drug addiction and compulsive behaviors have different neurophysiological bases. Although the fact that L-DOPA increases compulsive behaviors (although only in a fraction of the people who take it) indicates that dopamine is involved in compulsion, this seems to be an extension of its normal function rather than the radical and long-lasting alteration produced by addictive drugs.

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Semantics or neuroscience?

It is undeniable that some people develop a strong compulsion to gambling, watching porn, shopping, using social media, exercising, among other behaviors. Then, why not say that these behaviors are addictive?

Perhaps this is just a semantic problem. Whether these behaviors are addictive depends on how we define addiction. If it is defined simply as developing a strong need towards something, then these behaviors could be considered addictive. However, the evidence that I show here indicates that this compulsion is not mediated by dopamine in the reward pathway, which is the main goal of this article series.

In contrast, drug addiction is characterized by profound, long-lasting alterations in the reward pathway. This includes D2 downregulation in the reward pathway, which is produced by all addictive drugs and explains the impulsivity found in drug addicts. Moreover, many compulsive behaviors have opposite effects to addictive drugs on cross-sensitization with psychostimulants, psychostimulant self-administration, and reinstatement of drug-seeking behavior.

Giving the same name to two things with substantial neurophysiological signatures will lead to confusion. Therefore, I think it is better to reserve the name ‘addiction’ to substance use disorder, and to use ‘compulsion’ to name obsessive behaviors.

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What cause compulsive behaviors?

If compulsive behaviors are not caused by alterations in the reward pathway, then what causes them?

It could be that compulsive behaviors are just habits that are difficult to break. Habits are automatic behaviors triggered by clues in our environment. The reward pathway plays a role in learning the association between the clue and the behavior, but this happens with any habit, good or bad.

Social isolation, stress, boredom or strong beliefs may drive some individuals to focus on behaviors that provide excitement and relief from a pointless life. It is this decision that then recruits the reward pathway, so that these behaviors provide a pathological hyper-motivation and excessive focus on a single activity.

This is important because it shows that we cannot treat compulsive behaviors like drug addiction. What people need to come out of these compulsions is not guilt-trips, twelve steps programs or medications like methadone, naltrexone or buprenorphine. What they need is another source of motivation, to expand the scope of their lives, to find meaning elsewhere.

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Does pleasure decrease mental energy?

Circling back to the original question of this series of articles, the evidence I provided shows that sex and other forms of pleasure do not decrease our mental energy. Motivation and sustained effort are driven by the D2 receptors in the indirect pathway of the reward system and they are not downregulated by pleasure. In fact, some forms of pleasure, like exercise, playing or social interactions, increase the amount of D2 receptors and hence should increase our mental energy.

There is another problem with the ideas about dopamine in pop psychology. It is believed that pleasure produces ‘dopamine hits’. My next article will cover that at my substack.

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Previous articles in this series

Does Sex Deplete Our Mental Energy? (Wix, Medium, Substack, Fetlife).

Pleasure Electrodes in the Brain (Wix, Medium, Substack, Fetlife).

Can dopamine be depleted from its synapses? (Wix, Medium, Substack, Fetlife).

Dopamine D2 Receptor Downregulation Is the Hallmark of Addiction (Wix, Medium, Substack, Fetlife).

https://preview.redd.it/a1gb192f9btg1.png?width=817&format=png&auto=webp&s=715752af72590f1a91bd88c1ed922bea21e4dbd8

Note, this is a repost. Check them out here.

Okay so taking supplements , waking up early, eating good is all fine, but I feel like the single biggest wellness hack would be having positivity in your thoughts. The rest is all an extension and a thread of being positive.

So how does everyone manage to do this especially when things get crazy? And would you agree with what I said above?

I started looking into natural aphrodisiacs for men after realizing how anabolic testosterone is.

I was someone who probably had very low testosterone

The context is important; 3 years ago I was a full on junkie. I used drugs from my 13th til 27th, every day… I was highly functional so I didn’t have to quit; people didn’t notice. Addicted to smoking research chemical crystal drugs like N-ethyl pentedrone. I also took many benzodiazepines every day, for 7 years long.

My life was shit, my hormonal balance was even worse.

Right now i’ve been clean since October 2024. I started working out that month, 5 days per week. No days off. I’m still training; my body posture and entire look changed. I recently did bloodwork and am planning on doing it again in 5 months. Simply to prove the difference i already am. I will post again then, and refer to this post.

Here’s a list of supplements that seem to really work for me. Also I’ll mention the reason why I take it and what I believe it does for me.

Tongkat ali (Eurycoma Longifolia): lowers SHBG which in turn raises free testosterone.

Boron glycinate (only taking it 7 days, then abstaining for 2 weeks): lowers SHBG and raises free testosterone significantly.

Zinc citrate (25mg every 2 days):

- aromatase and alpha 5 reductase inhibition (positively impacts testosterone to estrogen conversion & testosterone to DHT conversion)

- also impacts SHBG positively possibly raising free testosterone

Magnesium citrate (400mg every day):

- lowers SHBG

- supports leydig cells

- it also raises general growth hormone levels like IGF-1

Pine pollen from Pinus Sylvestris and Pinus Massonia

- phyto androgens

- not well researched but feels incredibly powerful and accute/direct. I take 6grams of broken cell wall pollen in the morning.

I’m also taking stema tuberosa and polyalthia bullata but like the pine pollen this feels more like an experiment and i haven’t found extremely reliable data.

Now these supplements really helped me with erections and motivation in simple chores etc. But it also made my nipples puffy as hell, they itched and shit like that. So i researched why it happened; and it’s due to sudden raises in testosterone, your body converts it into estrogen and DHT. Through processes called aromatase and alpha 5 reductase.

So i started looking for supplements that downregulate this process and found 2 winners.

Indole 3 Carbinol:

- positively regulates aromatase and therefore the estrogen:testosterone ratio. It is really noticeable and around 30mg is enough to GREATLY amplify the effects of all the supplements named above.

- - stimulates conversion to 2-hydroxyestrone, a weaker/safer form of estrogen

- inhibits conversion to 16-alpha-hydroxyestrone; a strong estrogen linked to growth of cells and tissue etc.

Resveratrol:

- works as a “SERM” (Selective Estrogen Receptor Modulator) basically makes your body block negative effects estrogen whilst emulating the positive effects of estrogen.

- positively regulates aromatase

- inhibits alpha 5 reductase

- raises SHBG so probably best to take before taking the other SHBG lowering supplements

That’s just a substance I want to share I have recently discovered to improve one of the main factors in well-being: the teeth and oral hygiene also in relation to aging.

On a side note, plaque in the mouth is directly related to arterial plaque if it comes to chemical composition.

As well as plaque causing Alzheimer and dementia I think are fairly related.

For that reason not only brushing, flossing and stoking in important to do as a daily chore,

but certainly tongue scraping as well. I am always amazed how much ‘dirt’ is removed from the back of the tongue to the front on a daily basis.

Also the half year cleanup of tartar at the dentist for me is always surprising how much is actually still sedimented on the teeth. Wondering how diet is related to that.. the dentist doesn’t give an opinion about that understandably..

When I was 12 I was in a sports accident. Knocked the bottom half of my two front teeth. Had them replaced with porcelain crowns, no issues for 20 years.

I then decided to get braces at 27. They removed my wisdom teeth on both sides and 4 from the middle, 2 on each side. I then had braces for 20 months and then metal retainers. Then everything went down the drain.

The orthodontist missed a hole at the back of my left lower back tooth that was forming, saying that perhaps I had acid reflux which is why I had a plaque issue. They then said some of my teeth at the front needed fillings so I got 3 fillings. They finally found the hole that was close to becoming a root canal, but luckily not yet. I had a filling and the next thing I knew, I slowly started getting pain in my jaw joint on the left side. I saw a specialist who made me a TMJ splint and things got okay for a while but then I developed Eustachian Tube Disorder on the left side too. I now have a permanent hard lymph node on my left side in front of my ear (not cancerous). I'm at a loss. I do have lumbar scoliosis on the left side but super mild. I feel like something else is wrong here and would love some advice from any dental longevity folks. I brush with fluoride free toothpaste, chew xylitol gum after meals, floss, and pull with coconut oil when I remember. I also have a red light device for my teeth. Thanks so much.

Hello! I am hoping this community might be able to help me. I am going to be addressing biohacking with a class of mixed health profession students. While I do my best to keep up with developments, I was wondering what folks here think are the most relevant and important topics within biohacking that I should address? My goal is to help these students keep an open mind about this topic when they encounter future patients who may be interested in or participating in biohacking practices. Thank you in advance!

In lyophilised form?

I ended up buying like over 600IU of it and I don’t want to them to lose potency overtime, also would this apply to other peptides?

A couple days ago I felt a bad sore throat coming on so I went to an IV spa and got their cold/flu buster IV with extra glutathione and I decided to try a NAD+ injection because the nurse said it might help.

Ever since then I feel surges of energy, and I’ve had trouble getting to sleep at night, restless legs, etc. I had so much energy this afternoon I was worried I would make people uncomfortable to be around me!

I feel like I would’ve had a full on cold, and needed to rest and sleep these last few days, but instead of a sore throat, I have a slightly dry throat, and my ear is gurgling a little, but that’s the only symptom. My nose isn’t even congested.

Which ingredient likely did this to me? Or is it the combo of everything (vitamin C, B, etc. the glutathione and the NAD+)? Also, when will I return to my normal, slightly sluggish self? Not complaining, but this is pretty extreme, and I miss my afternoon naps. 😝

Has anyone transitioned from Reta to microdosing semiglutide for maintenance?