If you've been reading about natural remedies for hair loss, you may have come across an herb called saw palmetto. Sourced from the berries of a North American plant known as Serenoa repens or Sabal serrulata, saw palmetto extracts are said to help slow or reduce the type of hereditary hair loss known as androgenic alopecia (a common form of hair loss also known as male- or female-pattern baldness). Saw palmetto is sometimes touted as a natural treatment for other health conditions, such as acne, benign prostatic hyperplasia (BPH), erectile dysfunction (ED), and polycystic ovary syndrome (PCOS). Benefits for Hair Loss One theory on how saw palmetto might work is that it could 5-alpha-reductase, an enzyme involved in the conversion of the hormone testosterone to dihydrotestosterone (DHT). DHT is considered a key contributing factor to the onset and progression of androgenic alopecia. It is also said to increase the activity of an enzyme responsible for the metabolism of DHT into androstanediol (a weaker androgen hormone). Much of saw palmetto's popularity as a remedy for hair loss and baldness is based on how it is believed to work rather than on research. Although there is some laboratory research suggesting that saw palmetto has the potential to inhibit 5-alpha-reductase, there is a lack of well-designed clinical trials showing that saw palmetto can cause hair regrowth or stop the progression of hair loss. The available research includes an open-label study published in the International Journal of Immunopathology and Pharmacology in 2012. Of the 100 men with mild to moderate androgenic alopecia, one group took 320 mg of saw palmetto daily for 24 months, and the other group took 1 mg finasteride (a medication used for hair loss) daily for the same period. The researchers found that the hair growth score was higher in the group that received finasteride compared to the saw palmetto group, and that the effect of saw palmetto was inferior to that of finasteride. In a study published in the Journal of Alternative and Complementary Medicine in 2002, 26 men with mild to moderate androgenic alopecia took a supplement containing saw palmetto and beta-sitosterol or a placebo for 21 weeks. Treatment effectiveness at the final visit, assessed by staff, was reported to be 60 percent in the saw palmetto group compared to 11 percent in the placebo group. Side effects were mild and transient. Possible Side Effects As with other herbal supplements, little is known about the side effects of long-term use or high doses of saw palmetto. Side effects are usually mild. Stomach pain, constipation, diarrhea, nausea, and vomiting have been reported. Some men have reported sexual dysfunction. There is some concern that saw palmetto could cause liver, pancreatic, or cardiac problems in some people. There have been reports of liver injury and pancreatitis in people taking saw palmetto, however, there isn't enough information to know whether saw palmetto was the true cause of the adverse reactions. Although it hasn't been well-demonstrated in humans, saw palmetto may influence levels of sex hormones such as estrogen and testosterone. Until we know more, people with hormone-sensitive conditions, such as breast cancer, should avoid it. Also, saw palmetto could theoretically interfere with oral contraceptives and hormone therapy and may work in a similar manner to the medication finasteride. Children and pregnant or nursing women shouldn't take saw palmetto. Saw palmetto could slow blood clotting. People with bleeding disorders or who are taking anticoagulant or antiplatelet medications or supplements, such as warfarin (Coumadin®), aspirin, or clopidogrel (Plavix®), should avoid taking saw palmetto unless under medical supervision. It should also be avoided at least two weeks before and after surgery. It's important to keep in mind that supplements haven't been tested for safety and are largely unregulated. Make sure to read about using supplements safely. Using Saw Palmetto Losing your hair can be distressing. Although it may be tempting to start using saw palmetto, if you're considering using it, be sure to consult your health care provider to discuss whether it's appropriate for you. Most hair loss treatments require regular use, and it's important to consider the current lack of evidence or safety information (especially for long-term use). severe side effects Source: University of Bonn Summary: Hypotrichosis simplex leads to progressive hair loss starting in childhood. Geneticists have now deciphered a new gene that is responsible for this rare form of hair loss. Changes in the LSS gene lead to impairment of an important enzyme that has a crucial function in cholesterol metabolism.  Hypotrichosis simplex leads to progressive hair loss starting in childhood. A team of researchers led by human geneticists at the University Hospital of Bonn has now deciphered a new gene that is responsible for this rare form of hair loss. Changes in the LSS gene lead to impairment of an important enzyme that has a crucial function in cholesterol metabolism. The scientists now present their findings in the journal the American Journal of Human Genetics.
In infancy, fine hair tends to sprout sparsely. With increasing age, hair loss progresses. Ultimately, only a few hairs are left on the head and body. Hypotrichosis simplex is a rare form of hair loss (alopecia). The condition is limited to a few hundred families worldwide. So far, only a few genes are known that are causally related to the disease. Under the leadership of the Institute of Human Genetics at the University Hospital of Bonn, a team of researchers from Germany and Switzerland has now deciphered mutations in another gene that are responsible for hair loss. The scientists examined the coding genes of three families that are not related to each other and are of different ancestry. A total of eight relatives showed the typical symptoms of hair loss. All those affected had mutations in the LSS gene. "This gene encodes lanosterol synthase -- LSS for short," said Prof. Dr. Regina C. Betz from the Institute of Human Genetics at the University Hospital of Bonn. "The enzyme plays a key role in cholesterol metabolism." However, the cholesterol blood values of those affected are not changed. Betz: "There is an alternative metabolic pathway for cholesterol, which plays an important role in the hair follicle and is not related to blood cholesterol levels." Mutation leads to displacement of lanosterol synthase Using tissue samples, the scientists tried to find out exactly where the lanosterol synthase is located in the hair follicle cells. The hair roots are formed in the follicle. If the LSS gene is not mutated, the associated enzyme is located in a system of very fine channels in the follicle cells, the endoplasmic reticulum. If a mutation is present, the lanosterol synthase also spreads outside these channels into the adjacent substance, the cytosol. "We are not yet able to say why the hair is falling out," says lead author Maria-Teresa Romano, a doctoral student in Prof. Betz's team. "It is likely that the displacement of LSS from the endoplasmic reticulum results in a malfunction." Prof. Dr. Matthias Geyer from the Department of Structural Immunology at the University of Bonn investigated the consequences of mutations for the structure of the enzyme lanosterol synthase. With him and Prof. Betz, there are now two principal investigators from the Cluster of Excellence ImmunoSensation of the University of Bonn, which was impressively endorsed in the latest round of the Excellence Competition and will receive further funding. Improved diagnosis For the scientists, the current study result is an important finding: Each further gene decoded is yet another part of the jigsaw and helps to complete the picture of the biological basis of the disease. "A better understanding of the causes of the disease may in future enable new approaches to the treatment of hair loss," said the human geneticist. But there is still a long way to go. However, the discovery of the gene already contributes to an improved diagnosis of the rare disease. Betz: "Those affected by hypotrichosis simplex only have to deal with hair loss. This is upsetting, but other organs are not affected." Source: University of Alabama at Birmingham Summary: Researchers have reversed wrinkled skin and hair loss, hallmarks of aging, in a mouse model. When a mutation leading to mitochondrial dysfunction is induced, the mouse develops wrinkled skin and extensive, visible hair loss in a matter of weeks. When the mitochondrial function is restored by turning off the gene responsible for mitochondrial dysfunction, the mouse returns to smooth skin and thick fur, indistinguishable from a healthy mouse of the same age.  Wrinkled skin and hair loss are hallmarks of aging. What if they could be reversed?
Keshav Singh, Ph.D., and colleagues have done just that, in a mouse model developed at the University of Alabama at Birmingham. When a mutation leading to mitochondrial dysfunction is induced, the mouse develops wrinkled skin and extensive, visible hair loss in a matter of weeks. When the mitochondrial function is restored by turning off the gene responsible for mitochondrial dysfunction, the mouse returns to smooth skin and thick fur, indistinguishable from a healthy mouse of the same age. "To our knowledge, this observation is unprecedented," said Singh, a professor of genetics in the UAB School of Medicine. Importantly, the mutation that does this is in a nuclear gene affecting mitochondrial function, the tiny organelles known as the powerhouses of the cells. Numerous mitochondria in cells produce 90 percent of the chemical energy cells need to survive. In humans, a decline in mitochondrial function is seen during aging, and mitochondrial dysfunction can drive age-related diseases. A depletion of the DNA in mitochondria is also implicated in human mitochondrial diseases, cardiovascular disease, diabetes, age-associated neurological disorders and cancer. "This mouse model," Singh said, "should provide an unprecedented opportunity for the development of preventive and therapeutic drug development strategies to augment the mitochondrial functions for the treatment of aging-associated skin and hair pathology and other human diseases in which mitochondrial dysfunction plays a significant role." The mutation in the mouse model is induced when the antibiotic doxycycline is added to the food or drinking water. This causes depletion of mitochondrial DNA because the enzyme to replicate the DNA becomes inactive. In four weeks, the mice showed gray hair, reduced hair density, hair loss, slowed movements and lethargy, changes that are reminiscent of natural aging. Wrinkled skin was seen four to eight weeks after induction of the mutation, and females had more severe skin wrinkles than males. Dramatically, this hair loss and wrinkled skin could be reversed by turning off the mutation. The photos below show the hair loss and wrinkled skin after two months of doxycycline induction, and the same mouse a month later after doxycycline was stopped, allowing restoration of the depleted mitochondrial DNA. Little change was seen in other organs when the mutation was induced, suggesting an important role for mitochondria in skin compared to other tissues. The wrinkled skin showed changes similar to those seen in both intrinsic and extrinsic aging -- intrinsic aging is the natural process of aging, and extrinsic aging is the effect of external factors that influence aging, such as skin wrinkles that develop from excess sun or long-term smoking. Among the details, the skin of induced-mutation mice showed increased numbers of skin cells, abnormal thickening of the outer layer, dysfunctional hair follicles and increased inflammation that appeared to contribute to skin pathology. These are similar to extrinsic aging of the skin in humans. The mice with depleted mitochondrial DNA also showed changed expression of four aging-associated markers in cells, similar to intrinsic aging. The skin also showed disruption in the balance between matrix metalloproteinase enzymes and their tissue-specific inhibitor -- a balance of these two is necessary to maintain the collagen fibers in the skin that prevent wrinkling. The mitochondria of induced-mutation mice had reduced mitochondrial DNA content, altered mitochondrial gene expression, and instability of the large complexes in mitochondria that are involved in oxidative phosphorylation. Reversal of the mutation restored mitochondrial function, as well as the skin and hair pathology. This showed that mitochondria are reversible regulators of skin aging and loss of hair, an observation that Singh calls "surprising." "It suggests that epigenetic mechanisms underlying mitochondria-to-nucleus cross-talk must play an important role in the restoration of normal skin and hair phenotype," Singh said, who has a secondary UAB appointment as professor of pathology. "Further experiments are required to determine whether phenotypic changes in other organs can also be reversed to wildtype level by restoration of mitrochondrial DNA." |
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May 2024
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