It's Over Incel trait: you've never had sex but you experience UTIs and other dick issues

[sneed (not chuck)]

Man, fuck a UTI. I always get them, even when I shower regularly. They occur when I'm not on nofap. Feels like I need to pee all the time.

 

[Stupid Clown]

This is what jerking off since age six does to a man.

 

[PLA1092]

how

 

[Intellau_Celistic]

This is what jerking off since age six does to a man.

A hole told you this.

 

[Intellau_Celistic]

Yes. I've had repeated occurrences of H. Pylori. Mother would vomit from it when I was a child.

The role of the nuclear genome in maintaining the stability of the mitochondrial genome (mtDNA) is incompletely known. mtDNA sequence variants can exist in a state of heteroplasmy, which denotes the coexistence of organellar genomes with different sequences. Heteroplasmic variants that impair mitochondrial capacity cause disease, and the state of heteroplasmy itself is deleterious. However, mitochondrial heteroplasmy may provide an intermediate state in the emergence of novel mitochondrial haplogroups. We used genome-wide genotyping data from 982,072 European ancestry individuals to evaluate variation in mitochondrial heteroplasmy and to identify the regions of the nuclear genome that affect it. Age, sex, and mitochondrial haplogroup were associated with the extent of heteroplasmy. GWAS identified 20 loci for heteroplasmy that exceeded genome-wide significance. This included a region overlapping mitochondrial transcription factor A (TFAM), which has multiple roles in mtDNA packaging, replication, and transcription. These results show that mitochondrial heteroplasmy has a heritable nuclear component.

Mitochondria carry multiple copies of their own genome organized into nucleoids, which include the nuclear-encoded DNA polymerase γ (POLG) and transcription factor A (TFAM)19. TFAM also helps maintaining mitochondrial DNA (mtDNA) integrity. We previously reported that H. pylori induces mtDNA mutations in gastric epithelial cells, also observed in gastritis patients, indicating an early occurrence of mtDNA instability during disease progression20. H. pylori also impairs mtDNA repair pathways.

Mitochondria are essential organelles not only responsible for energy production but also involved in apoptosis, calcium homeostasis, lipids and amino acids metabolism. Targeting mitochondria has emerged as a key strategy for bacteria to hijack host cells physiology and promote infection1,2. However, the underlying mechanisms and their relevance to disease remain to a great extent unresolved. Virulence factors of both intracellular and extracellular bacteria are secreted in the host cells and may interact with mitochondria, leading to modulation of mitochondrial function and ultimately promoting pathogenesis3,4,5. Mitochondria have also been reported as modulators of cellular antibacterial immunity and inflammatory response6. Helicobacter pylori is a human gastric pathogen and a major risk factor for gastric cancer7,8. H. pylori damages gastric cells introducing genetic instability and mitochondrial dysfunction, which largely contribute to the infection-associated pathogenicity9,10,11,12.

Mitochondria carry multiple copies of their own genome organized into nucleoids, which include the nuclear-encoded DNA polymerase γ (POLG) and transcription factor A (TFAM)19. TFAM also helps maintaining mitochondrial DNA (mtDNA) integrity. We previously reported that H. pylori induces mtDNA mutations in gastric epithelial cells, also observed in gastritis patients, indicating an early occurrence of mtDNA instability during disease progression20. H. pylori also impairs mtDNA repair pathways21.

Helicobacter pylori targets mitochondrial import and components of mitochondrial DNA replication machinery through an alternative VacA-dependent and a VacA-independent mechanisms - Scientific Reports

Targeting mitochondria is a powerful strategy for pathogens to subvert cell physiology and establish infection. Helicobacter pylori is a bacterial pathogen associated with gastric cancer development that is known to target mitochondria directly and exclusively through its pro-apoptotic and...

www.nature.com

 

[Puppeter]

I pee a lot but its metabolism i think

 

[Intellau_Celistic]

Anecdote:

Understood.

When I was in my early teens, my father would constantly denigrate my autistic traits. He would often tell me,

"Why are you so shameful all the time?" (I was anxious and kept my head down in public)

"We're going to grandma's house, hurry up!"(He wanted to make himself seem like an excellent father by showing her his son)

"You're moving so slowly"(He would hit me; I was sluggish from ASD/trauma)

"Your cousins are better than you!" (Again, anxiety and depression)

"I'm saying this to be kind. Don't anger me." (If I was struggling to go inside a store due to anxiety)

I once had Pyelonephritis and was fairly weak from it to the point of needing to stay home when my father wanted to visit a store. My father, instead of asking me if I took my prescribed antibiotics, simply told me, "Hurry up, let's go see grandma". He then asked Grandma to patronize me for my "disobedience".

I temporarily walked outside with my half-relatives in 2013...I stopped after I developed Pyelonephritis and realized I didn't respect them much.

 

[Immolator]

i can’t pull back my foreskin + dicklet, so I’m screwed

 

[Saint Cho]

how

This. Literally how unless you stick your cock in nasty places.

 

[Stupid Clown]

A hole told you this.

No, I've been jerking off or at least edging since age 6.

 

[Anthrax]

This. Literally how unless you stick your cock in nasty places.

I shower 1-2 times a week and have never had issues. Seems like op might be a sex-haver

 

[NorwoodVictim]

Nah, just a small dick

 

[subhuman]

I don’t have a frenulum