squeegee
Banned
- Reaction score
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Serum lipoprotein (a) as an atherosclerosis risk factor in
men with androgenic alopecia
www.iranjd.ir/download.asp?code=IJD11145781
Results
The mean age of the cases and the controls was
25.7 ± 6.26 and 27.16 ± 6.46 years, respectively with
no significant difference between the two groups.
The mean age of the patients with frontal and vertex
baldness was 23.35 and 28.35 years, respectively
(p<0.05). Table 1 shows the family history of Androgenetic Alopecia,
HTN, DM and CAD in the case and control groups.
As this table shows, a positive family history of
Androgenetic Alopecia and CAD was significantly more frequent in
cases than the controls (P < 0.05). The pattern of
hair loss was compatible with Hamilton pattern
in 91.5% of all cases; 53.6% had frontal recession
and 46.4% had vertex loss pattern; 2.1% of the
patients had the Ludwig pattern hair loss and in
6.4%, the pattern was undetermined.
Table 2 shows the levels of total serum cholesterol,
triglyceride, HDL–cholesterol, LDL–cholesterol,
LP (a), Apo A1 and Apo B. As it is shown in the
table, the level of LP (a) was significantly higher
in patients than controls (P < 0.001). 38.6% of the
patients and only 4.4 % of the controls had an LP(a)
level more than 30 mg/dl, which is the critical
level for atherosclerosis (P < 0.001). The level of LP
(a) was not significantly different in the alopecia
subgroups; frontal only baldness vs. vertex baldness.
There were no statistically significant differences
in the mean levels of cholesterol, triglyceride, LDL,
HDL–cholesterol, Apo A and Apo B between the
patients and the controls.
- - - Updated - - -
LP(a) is genetic and pretty much the only 2 balding species harbour LP(a)... which makes it very interesting...
from Wiki..
The physiological function of Lp(a)/apo(a) is still unknown. A function within the coagulation system seems plausible, given the aspect of the high homology between apo(a) and plasminogen.[SUP][7][/SUP] In fact, the LPA gene derives from a duplication of the plasminogen gene.
Other functions have been related to recruitment of inflammatory cells through interaction with Mac-1 integrin, angiogenesis, and wound healing.
However, individuals without Lp(a) or with very low Lp(a) levels seem to be healthy. Thus plasma Lp(a) is certainly not vital, at least under normal environmental conditions. Since apo(a)/Lp(a) derived rather recently in mammalian evolution - only old world monkeys and humans have been shown to harbour Lp(a) - its function might not be vital but just evolutionarily advantageous under certain environmental conditions, e.g. in case of exposure to certain infectious diseases.
Another possibility, suggested by Linus Pauling, is that Lp(a) is a primate adaptation to L-gulonolactone oxidase (GULO) deficiency, who thought that found only in certain lines of mammals. GULO is required for converting glucose to ascorbic acid (vitamin C), which is needed to repair arteries; following the loss of GULO, those primates that adopted diets less abundant in vitamin C may have used Lp(a) as an ascorbic-acid surrogate to repair arterial walls.[SUP][16][/SUP]
men with androgenic alopecia
www.iranjd.ir/download.asp?code=IJD11145781
Results
The mean age of the cases and the controls was
25.7 ± 6.26 and 27.16 ± 6.46 years, respectively with
no significant difference between the two groups.
The mean age of the patients with frontal and vertex
baldness was 23.35 and 28.35 years, respectively
(p<0.05). Table 1 shows the family history of Androgenetic Alopecia,
HTN, DM and CAD in the case and control groups.
As this table shows, a positive family history of
Androgenetic Alopecia and CAD was significantly more frequent in
cases than the controls (P < 0.05). The pattern of
hair loss was compatible with Hamilton pattern
in 91.5% of all cases; 53.6% had frontal recession
and 46.4% had vertex loss pattern; 2.1% of the
patients had the Ludwig pattern hair loss and in
6.4%, the pattern was undetermined.
Table 2 shows the levels of total serum cholesterol,
triglyceride, HDL–cholesterol, LDL–cholesterol,
LP (a), Apo A1 and Apo B. As it is shown in the
table, the level of LP (a) was significantly higher
in patients than controls (P < 0.001). 38.6% of the
patients and only 4.4 % of the controls had an LP(a)
level more than 30 mg/dl, which is the critical
level for atherosclerosis (P < 0.001). The level of LP
(a) was not significantly different in the alopecia
subgroups; frontal only baldness vs. vertex baldness.
There were no statistically significant differences
in the mean levels of cholesterol, triglyceride, LDL,
HDL–cholesterol, Apo A and Apo B between the
patients and the controls.
- - - Updated - - -
LP(a) is genetic and pretty much the only 2 balding species harbour LP(a)... which makes it very interesting...
from Wiki..
The physiological function of Lp(a)/apo(a) is still unknown. A function within the coagulation system seems plausible, given the aspect of the high homology between apo(a) and plasminogen.[SUP][7][/SUP] In fact, the LPA gene derives from a duplication of the plasminogen gene.
Other functions have been related to recruitment of inflammatory cells through interaction with Mac-1 integrin, angiogenesis, and wound healing.
However, individuals without Lp(a) or with very low Lp(a) levels seem to be healthy. Thus plasma Lp(a) is certainly not vital, at least under normal environmental conditions. Since apo(a)/Lp(a) derived rather recently in mammalian evolution - only old world monkeys and humans have been shown to harbour Lp(a) - its function might not be vital but just evolutionarily advantageous under certain environmental conditions, e.g. in case of exposure to certain infectious diseases.
Another possibility, suggested by Linus Pauling, is that Lp(a) is a primate adaptation to L-gulonolactone oxidase (GULO) deficiency, who thought that found only in certain lines of mammals. GULO is required for converting glucose to ascorbic acid (vitamin C), which is needed to repair arteries; following the loss of GULO, those primates that adopted diets less abundant in vitamin C may have used Lp(a) as an ascorbic-acid surrogate to repair arterial walls.[SUP][16][/SUP]
