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Category: sex

In this study, we have demonstrated the crucial role of NAD+ homeostasis, particularly through the de novo synthesis pathway mediated by Qprt, in maintaining spermatogenesis with age. The deletion of Qprt led to progressive declines in NAD+ levels, particularly after 6 months of age, which were associated with significant defects in germ cell survival and mitochondrial function in spermatocytes. These disruptions manifested as impaired progression through meiosis, defective DNA double-strand break repair, and abnormal meiotic sex chromosome inactivation. Our findings also highlight the therapeutic potential of NAD+ precursor supplementation, as nicotinamide riboside effectively rescued the observed spermatogenic abnormalities in Qprt-deficient mice, emphasizing the importance of NAD+ in reproductive health and aging.

NAD+ can be synthesized through three pathways: the Preiss-Handler pathway, the salvage pathway, and the de novo pathway (Liu et al. 2018 ; Harjes 2019). In the de novo pathway, the essential amino acid tryptophan serves as a substrate, with Qprt catalyzing the formation of nicotinic acid mononucleotide, which is subsequently converted into NAD+ via a series of enzymatic reactions in the Preiss-Handler pathway. Coordinated regulation of these three pathways is crucial for maintaining intracellular NAD+ levels, which are essential for cellular function, a decline in NAD+ levels can lead to various pathological and physiological conditions (Minhas et al. 2019 ; Zhang et al. 2019a). In this study, we identified that Qprt, the rate-limiting enzyme in the NAD+ de novo synthesis pathway, is predominantly expressed in spermatocytes within the testes.

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Bolstered by Silicon Valley investment, scientists are making such rapid progress that lab-grown human eggs and sperm could be a reality within a decade, a meeting of the Human Fertilisation and Embryology Authority board heard last week.

In-vitro gametes (IVGs), eggs or sperm that are created in the lab from genetically reprogrammed skin or stem cells, are viewed as the holy grail of fertility research.

The technology promises to remove age barriers to conception and could pave the way for same-sex couples to have biological children together. It also poses unprecedented medical and ethical risks, which the HFEA now believes need to be considered in a proposed overhaul of fertility laws.

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Subtle activation of a small subset of neurons in one region of the brain can make male mice resilient to, and even reverse, the detrimental effects of chronic stress. The same is true for female mice, but in a totally different region of the brain.

Researchers at Penn State reported these findings in two studies published in the journal Molecular Psychiatry and said the results could help explain the efficacy, or lack thereof, of certain antidepressant drugs and inform the development of new drugs and therapies.

The team developed a protocol to continuously activate neurons that produce the signaling molecule somatostatin, which helps regulate several biological processes, in specific brain regions in mice. The researchers found that doing so in a region of the brain called the prelimbic cortex made male mice resilient to stress, but failed to do so in female mice.

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Gray matter is made up of neuron cell bodies and dendrites and is responsible for processing and interpreting information, such as sensation, perception, learning, speech, and cognition. White matter is made up of axons, which are long nerve fibers that connect neurons together from different parts of the brain.

In the study, male brains tended to be greater in volume than female brains. When adjusted for total brain volume, female infants on average had significantly more , while on average had significantly more in their brains.

Yumnah Khan, a Ph.D. student at the Autism Research Center at the University of Cambridge, who led the study, said, Our study settles an age-old question of whether male and female brains differ at birth. We know there are differences in the brains of older children and adults, but our findings show that they are already present in the earliest days of life.

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Meanwhile, scientists dug into how psychedelics and MDMA fight off depression and post-traumatic stress disorders. The year was a relative setback for the psychedelic renaissance, with the FDA rejecting MDMA therapy. But the field is still gaining recognition for its therapeutic potential.

Then there’s lenacapavir, a shot that protects people from HIV. Named “breakthrough of the year” by Science, the shot completely protected African teenage girls and women against HIV infection. Another trial supported the results, showing the drug protected people who have sex with men at nearly 100 percent efficacy. The success stems from a new understanding of the protein “capsule” guarding the virus’ genetic material. Many other viruses have a similar makeup—meaning the strategy could help researchers design new drugs to fight them off too.

So, what’s poised to take the leap from breakthrough to clinical approval in 2025? Here’s what to expect in the year ahead.

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DOI: Abstract We are living in a historical period in respect to the deterioration in public health, as we experience the rise of the catastrophic obesity epidemic and mental health crisis in recent decades, despite the great efforts from the scientific and medical community to seek health solutions and to try to find cures to the enormous human suffering and economic costs resulting by this collapse in public health. This trend has reached such a critical level that it jeopardizes society when over 40% of the population is obese in the United States, suffering grave medical health conditions, even as the expenditure on public health is rising exponentially to over 20% of gross domestic product. This should point to a monumental failure in our fundamental understanding of basic human biology and health. This article suggests that our current Western reductionist scientific paradigm in both biology and medicine has proved impotent and failed us completely. Therefore, the current cultural health crises require a more holistic approach to human biology and health in terms of chronobiological trends. The emerging neuroscience of brain energy metabolism will be considered as a holistic model for understanding how solar cycles affect our civilization and drive our sex and growth hormones and neurotransmitters that shape both our physical and mental health.

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Aging happens in distinct stages marked by synchronized cellular changes across organs, as shown in Rockefeller’s largest-ever mammalian aging atlas. Their findings offer clues for targeting aging processes and reveal key age and sex differences in cellular dynamics.

If you compared photos of a maple tree taken in July and December, the difference would be striking: a vibrant green canopy in summer versus bare, stark branches in winter. What those images wouldn’t reveal is how the transformation unfolded—whether it was gradual or sudden. In reality, deciduous trees usually wait for environmental cues, such as changes in light or temperature, before shedding all their leaves within a brief span of one to two weeks.

When it comes to aging, we may be more like these trees than we realized.

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By Sher Bahadur Poudel & Shoshana Yakar et al.

Several mouse lines with congenital growth hormone (GH)/insulin-like growth factor-1 (IGF-1) axis disruption have shown improved health and extended lifespan. The current study investigated how inactivating this axis, specifically during aging, impacts the healthspan. We used a tamoxifen-inducible global GH receptor (GHR) knockout mouse model starting at 12 months and followed the mice until 24 months of age (iGHRKO12–24 mice). We found sex-and tissue-specific effects, with some being pro-aging and others anti-aging. Measuring an array of cytokines in serum revealed that inactivation of the GH/IGF-1 axis at 12 months did not affect systemic inflammation during aging. On the other hand, hypothalamic inflammation was significantly reduced in iGHRKO12–24 mice, evidenced by GFAP+ (glial fibrillary acidic protein, a marker of astrocytes) and Iba-1+ (a marker for microglia). Liver RNAseq analysis indicated feminization of the male transcriptome, with significant changes in the expression of monooxygenase, sulfotransferase, and solute-carrier-transporter gene clusters. Finally, we found impaired bone morphology, more pronounced in male iGHRKO12–24 mice and correlated with GH/IGF-1 inactivation onset age. We conclude that inhibiting the GH/IGF-1 axis during aging only partially preserves the beneficial healthspan effects observed with congenital GH deficiency.

Inactivating the GH axis during aging has sex-and tissue-specific effects on healthspan. Deleting the GH receptor (GHR) in the entire body at 12 months of age led to feminizing the male liver transcriptome, significantly altering the expression of p450 and sulfotransferase gene clusters. While GHR deletion during aging did not impact systemic inflammation, it was linked to reduced hypothalamic inflammation. Additionally, we observed impaired bone morphology, particularly in male mice, which correlated with the age at which GH/IGF-1 inactivation began. Our findings suggest that inhibiting the GH axis during aging only partially maintains the beneficial healthspan effects seen with congenital GH deficiency.

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