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	<title>Comments for </title>
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	<link>http://www.cenegenicsfoundation.org/blog</link>
	<description></description>
	<lastBuildDate>Tue, 13 Jul 2010 17:17:41 -0500</lastBuildDate>
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		<title>Comment on Telomeres &amp; CA by Dirkparvus</title>
		<link>http://www.cenegenicsfoundation.org/blog/?p=802&#038;cpage=1#comment-1017</link>
		<dc:creator>Dirkparvus</dc:creator>
		<pubDate>Tue, 13 Jul 2010 17:17:41 +0000</pubDate>
		<guid isPermaLink="false">http://www.cenegenicsfoundation.org/blog/?p=802#comment-1017</guid>
		<description>Now with TA65 available, if we increase our Telomere length using TA65 do you think we will get the same benefits? Probably no studies available to give us the answer.</description>
		<content:encoded><![CDATA[<p>Now with TA65 available, if we increase our Telomere length using TA65 do you think we will get the same benefits? Probably no studies available to give us the answer.</p>
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		<title>Comment on Is TOM the male equivalent of WHI? by Mickey Barber, MD</title>
		<link>http://www.cenegenicsfoundation.org/blog/?p=797&#038;cpage=1#comment-963</link>
		<dc:creator>Mickey Barber, MD</dc:creator>
		<pubDate>Tue, 06 Jul 2010 20:39:37 +0000</pubDate>
		<guid isPermaLink="false">http://www.cenegenicsfoundation.org/blog/?p=797#comment-963</guid>
		<description>I can&#039;t imagine why in this or any study twith he investigators knowing that estradiol may have a negative impact on CV function wouldn&#039;t measure it! It would also have been interesting to measure some inflammatory markers like CRP. Also, how can peripheral edema be considered a serious CV event when the etiology is not clear/stated? Certainly the variety of &quot;serious cardiovascular events&quot; makes these results less compelling.</description>
		<content:encoded><![CDATA[<p>I can&#8217;t imagine why in this or any study twith he investigators knowing that estradiol may have a negative impact on CV function wouldn&#8217;t measure it! It would also have been interesting to measure some inflammatory markers like CRP. Also, how can peripheral edema be considered a serious CV event when the etiology is not clear/stated? Certainly the variety of &#8220;serious cardiovascular events&#8221; makes these results less compelling.</p>
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		<title>Comment on Is TOM the male equivalent of WHI? by Paul Ogden, MD, MSPH</title>
		<link>http://www.cenegenicsfoundation.org/blog/?p=797&#038;cpage=1#comment-931</link>
		<dc:creator>Paul Ogden, MD, MSPH</dc:creator>
		<pubDate>Thu, 01 Jul 2010 19:37:35 +0000</pubDate>
		<guid isPermaLink="false">http://www.cenegenicsfoundation.org/blog/?p=797#comment-931</guid>
		<description>Alvin, good article. I looked back at the previous article you quoted, and interestingly there is twice as many adverse events in that treatment group.  
&quot;There were three serious adverse events in the placebo
(prostate cancer, acute myocardial infarction, and
death from ruptured abdominal aortic aneurysm) and six
serious adverse events in the T group (lung cancer, esophagus
cancer, pulmonary embolism, heart failure, abdominal
aneurysm, and constrictive pericarditis).
Again, small numbers, and such a scattered bunch of diseases that it would be hard to pose a consitent pathophysiology.     
I don&#039;t think the answer is here regarding safety overall, but the response in strength is unequivocal.    Cenegenics needs to publish our data, even though it is not randomized, controlled or prospective, a series of 15,000 patients would be compelling.</description>
		<content:encoded><![CDATA[<p>Alvin, good article. I looked back at the previous article you quoted, and interestingly there is twice as many adverse events in that treatment group.<br />
&#8220;There were three serious adverse events in the placebo<br />
(prostate cancer, acute myocardial infarction, and<br />
death from ruptured abdominal aortic aneurysm) and six<br />
serious adverse events in the T group (lung cancer, esophagus<br />
cancer, pulmonary embolism, heart failure, abdominal<br />
aneurysm, and constrictive pericarditis).<br />
Again, small numbers, and such a scattered bunch of diseases that it would be hard to pose a consitent pathophysiology.<br />
I don&#8217;t think the answer is here regarding safety overall, but the response in strength is unequivocal.    Cenegenics needs to publish our data, even though it is not randomized, controlled or prospective, a series of 15,000 patients would be compelling.</p>
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		<title>Comment on Is TOM the male equivalent of WHI? by Julie McCallen</title>
		<link>http://www.cenegenicsfoundation.org/blog/?p=797&#038;cpage=1#comment-929</link>
		<dc:creator>Julie McCallen</dc:creator>
		<pubDate>Thu, 01 Jul 2010 18:35:27 +0000</pubDate>
		<guid isPermaLink="false">http://www.cenegenicsfoundation.org/blog/?p=797#comment-929</guid>
		<description>Dear Alvin,

 

When I read your note I thought of my oldest man on the program – he is now 86.  When he started at about age 82, he was near death.  Now he has completely regained cognitive function, energy, balance, vigor, and humor.  It would be terrific if we, as Cenegenics, could publish data to counter TOM.

Julie</description>
		<content:encoded><![CDATA[<p>Dear Alvin,</p>
<p>When I read your note I thought of my oldest man on the program – he is now 86.  When he started at about age 82, he was near death.  Now he has completely regained cognitive function, energy, balance, vigor, and humor.  It would be terrific if we, as Cenegenics, could publish data to counter TOM.</p>
<p>Julie</p>
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		<title>Comment on Factor V Leiden Deficiency by Earl Eye MD</title>
		<link>http://www.cenegenicsfoundation.org/blog/?p=445&#038;cpage=1#comment-881</link>
		<dc:creator>Earl Eye MD</dc:creator>
		<pubDate>Wed, 23 Jun 2010 16:53:52 +0000</pubDate>
		<guid isPermaLink="false">http://www.cenegenicsfoundation.org/blog/?p=445#comment-881</guid>
		<description>To complete my above post-Circulation. 2005; 112:3495-3500, Prothromboitc mutations, Hormone Therapy and DVT Among Post monopausal Women.
TABLE 2. OR of VTE in Relation to the Presence of 1 Prothrombotic Mutation or Estrogen Use
________________________________________	Patients (n=235), n (%)
________________________________________	Controls (n=554), n (%)
________________________________________	OR (95%CI)
________________________________________
			Crude
________________________________________	Adjusted*
________________________________________
Estrogen therapy				
    Nonuse 
124 (52.8)	341 (61.6)	1	1
    Oral estrogen use	51 (21.7)	44 (7.9)	3.2  (2.0–5.0)	4.3  (2.6–7.2)
    Transdermal estrogen use	60 (25.5)	169 (30.5)	1.0 (0.7–1.4)	1.2&#124;&#124; (0.8–1.7)
Factor V Leiden				
    GG	200 (85.1)	527 (95.1)	1	1
    AG or AA	35 (14.9)	27 (4.9)	3.4  (2.0–5.8)	3.2¶ (1.8–5.5)
Prothrombin G20210A				
    GG	209 (88.9)	540 (97.5)	1	1
    AG or AA	26 (11.1)	14 (2.5)	4.8  (2.5–9.4)	4.8¶ (2.6–10.3)
________________________________________
*Adjusted for age, center, and BMI.
 Nonusers include never and past users.

 P&lt;0.0001.

 P&lt;0.0001, also adjusted for prothrombotic mutation.

&#124;&#124;P=NS, also adjusted for prothrombotic mutation.
¶P&lt;0.0001, also adjusted for oral estrogen use.</description>
		<content:encoded><![CDATA[<p>To complete my above post-Circulation. 2005; 112:3495-3500, Prothromboitc mutations, Hormone Therapy and DVT Among Post monopausal Women.<br />
TABLE 2. OR of VTE in Relation to the Presence of 1 Prothrombotic Mutation or Estrogen Use<br />
________________________________________	Patients (n=235), n (%)<br />
________________________________________	Controls (n=554), n (%)<br />
________________________________________	OR (95%CI)<br />
________________________________________<br />
			Crude<br />
________________________________________	Adjusted*<br />
________________________________________<br />
Estrogen therapy<br />
    Nonuse<br />
124 (52.8)	341 (61.6)	1	1<br />
    Oral estrogen use	51 (21.7)	44 (7.9)	3.2  (2.0–5.0)	4.3  (2.6–7.2)<br />
    Transdermal estrogen use	60 (25.5)	169 (30.5)	1.0 (0.7–1.4)	1.2|| (0.8–1.7)<br />
Factor V Leiden<br />
    GG	200 (85.1)	527 (95.1)	1	1<br />
    AG or AA	35 (14.9)	27 (4.9)	3.4  (2.0–5.8)	3.2¶ (1.8–5.5)<br />
Prothrombin G20210A<br />
    GG	209 (88.9)	540 (97.5)	1	1<br />
    AG or AA	26 (11.1)	14 (2.5)	4.8  (2.5–9.4)	4.8¶ (2.6–10.3)<br />
________________________________________<br />
*Adjusted for age, center, and BMI.<br />
 Nonusers include never and past users.</p>
<p> P&lt;0.0001.</p>
<p> P&lt;0.0001, also adjusted for prothrombotic mutation.</p>
<p>||P=NS, also adjusted for prothrombotic mutation.<br />
¶P&lt;0.0001, also adjusted for oral estrogen use.</p>
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		<title>Comment on Factor V Leiden Deficiency by Earl Eye MD</title>
		<link>http://www.cenegenicsfoundation.org/blog/?p=445&#038;cpage=1#comment-880</link>
		<dc:creator>Earl Eye MD</dc:creator>
		<pubDate>Wed, 23 Jun 2010 16:50:17 +0000</pubDate>
		<guid isPermaLink="false">http://www.cenegenicsfoundation.org/blog/?p=445#comment-880</guid>
		<description>There does appear to be a low risk of increase in DVT in patients with coagulation factor issues. The data from the American Heart Association Journal in 2005 does not reflect the very high risk.</description>
		<content:encoded><![CDATA[<p>There does appear to be a low risk of increase in DVT in patients with coagulation factor issues. The data from the American Heart Association Journal in 2005 does not reflect the very high risk.</p>
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		<title>Comment on Factor V Leiden Deficiency by Estrogen &#38; Progesterone in Menopausse &#171;</title>
		<link>http://www.cenegenicsfoundation.org/blog/?p=445&#038;cpage=1#comment-877</link>
		<dc:creator>Estrogen &#38; Progesterone in Menopausse &#171;</dc:creator>
		<pubDate>Tue, 22 Jun 2010 23:51:11 +0000</pubDate>
		<guid isPermaLink="false">http://www.cenegenicsfoundation.org/blog/?p=445#comment-877</guid>
		<description>[...] sexual function. HT increases risk of thromboembolic events (but don’t forget to look over my 2/13/08 &amp; 2/20/08 posts) and doesn’t improve cognition when initiated after 60yo while E alone w/o P [...]</description>
		<content:encoded><![CDATA[<p>[...] sexual function. HT increases risk of thromboembolic events (but don’t forget to look over my 2/13/08 &amp; 2/20/08 posts) and doesn’t improve cognition when initiated after 60yo while E alone w/o P [...]</p>
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		<title>Comment on Sugar vs Cholesterol: What&#8217;s the link? by Jack Kruse</title>
		<link>http://www.cenegenicsfoundation.org/blog/?p=752&#038;cpage=1#comment-867</link>
		<dc:creator>Jack Kruse</dc:creator>
		<pubDate>Sun, 20 Jun 2010 22:17:16 +0000</pubDate>
		<guid isPermaLink="false">http://www.cenegenicsfoundation.org/blog/?p=752#comment-867</guid>
		<description>alvin......take a look at this study.

new study in the journal Obesity, by Y. Li and colleagues, showed that compared to a placebo, a low-dose multivitamin caused obese volunteers to lose 7 lb (3.2 kg) of fat mass in 6 months, mostly from the abdominal region (4). The supplement also reduced LDL by 27%, increased HDL by a whopping 40% and increased resting energy expenditure. Here&#039;s what the supplement contained:

Vitamin A(containing natural mixed b-carotene) 5000 IU
Vitamin D 400 IU
Vitamin E 30 IU
Thiamin 1.5 mg
Riboflavin 1.7 mg
Vitamin B6 2 mg
Vitamin C 60 mg
Vitamin B12 6 mcg
Vitamin K1 25 mcg
Biotin 30 mcg
Folic acid 400 mcg
Nicotinamide 20 mg
Pantothenic acid 10 mg
Calcium 162 mg
Phosphorus 125 mg
Chlorine 36.3 mg
Magnesium 100 mg
Iron 18 mg
Copper 2 mg
Zinc 15 mg
Manganese 2.5 mg
Iodine 150 mcg
Chromium 25 mcg
Molybdenum 25 mcg
Selenium 25 mcg
Nickel 5 mcg
Stannum 10 mcg
Silicon 10 mcg
Vanadium 10 mcg</description>
		<content:encoded><![CDATA[<p>alvin&#8230;&#8230;take a look at this study.</p>
<p>new study in the journal Obesity, by Y. Li and colleagues, showed that compared to a placebo, a low-dose multivitamin caused obese volunteers to lose 7 lb (3.2 kg) of fat mass in 6 months, mostly from the abdominal region (4). The supplement also reduced LDL by 27%, increased HDL by a whopping 40% and increased resting energy expenditure. Here&#8217;s what the supplement contained:</p>
<p>Vitamin A(containing natural mixed b-carotene) 5000 IU<br />
Vitamin D 400 IU<br />
Vitamin E 30 IU<br />
Thiamin 1.5 mg<br />
Riboflavin 1.7 mg<br />
Vitamin B6 2 mg<br />
Vitamin C 60 mg<br />
Vitamin B12 6 mcg<br />
Vitamin K1 25 mcg<br />
Biotin 30 mcg<br />
Folic acid 400 mcg<br />
Nicotinamide 20 mg<br />
Pantothenic acid 10 mg<br />
Calcium 162 mg<br />
Phosphorus 125 mg<br />
Chlorine 36.3 mg<br />
Magnesium 100 mg<br />
Iron 18 mg<br />
Copper 2 mg<br />
Zinc 15 mg<br />
Manganese 2.5 mg<br />
Iodine 150 mcg<br />
Chromium 25 mcg<br />
Molybdenum 25 mcg<br />
Selenium 25 mcg<br />
Nickel 5 mcg<br />
Stannum 10 mcg<br />
Silicon 10 mcg<br />
Vanadium 10 mcg</p>
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		<title>Comment on News from ACC: How (Not) to Prevent DM &amp; CV Events by Jack Kruse</title>
		<link>http://www.cenegenicsfoundation.org/blog/?p=718&#038;cpage=1#comment-865</link>
		<dc:creator>Jack Kruse</dc:creator>
		<pubDate>Sun, 20 Jun 2010 15:34:26 +0000</pubDate>
		<guid isPermaLink="false">http://www.cenegenicsfoundation.org/blog/?p=718#comment-865</guid>
		<description>Alvin it is not surpising at all to me because if we all go back and open up our biochemistry books the end point of carbohydrate metabolism is VLDL cholesterol and uric acid.  The shocking thing is that American medicine still believes the lipid hypothesis when science has always told us it is the carbs that drive the VLDL train.  Saturated fats have nothing to do with heart disease or cholesterol levels either.  The uric acid level elevations are what ultimately cause gout and hypertension in our patients.  That is why it is imperitive we keep their insulin levels low get them to master leptin sensitivity and keep them as far away from refined carbs as possible.  In our country today they are being fed a diet of nothing but refined corn syrup and grains loaded in omega six and nine&#039;s.</description>
		<content:encoded><![CDATA[<p>Alvin it is not surpising at all to me because if we all go back and open up our biochemistry books the end point of carbohydrate metabolism is VLDL cholesterol and uric acid.  The shocking thing is that American medicine still believes the lipid hypothesis when science has always told us it is the carbs that drive the VLDL train.  Saturated fats have nothing to do with heart disease or cholesterol levels either.  The uric acid level elevations are what ultimately cause gout and hypertension in our patients.  That is why it is imperitive we keep their insulin levels low get them to master leptin sensitivity and keep them as far away from refined carbs as possible.  In our country today they are being fed a diet of nothing but refined corn syrup and grains loaded in omega six and nine&#8217;s.</p>
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		<title>Comment on Vitamin B6 vs Colorectal CA (Thank you, Cicely!) by Vitamin B6 vs Lung CA &#171;</title>
		<link>http://www.cenegenicsfoundation.org/blog/?p=726&#038;cpage=1#comment-837</link>
		<dc:creator>Vitamin B6 vs Lung CA &#171;</dc:creator>
		<pubDate>Thu, 17 Jun 2010 01:55:29 +0000</pubDate>
		<guid isPermaLink="false">http://www.cenegenicsfoundation.org/blog/?p=726#comment-837</guid>
		<description>[...] it&#8217;s been fascinating to follow the story lately of B vitamins, especially B6. On March 19th, I reviewed a study that linked more B6 to less colon CA. Yet on April 28th, I reviewed a study [...]</description>
		<content:encoded><![CDATA[<p>[...] it&#8217;s been fascinating to follow the story lately of B vitamins, especially B6. On March 19th, I reviewed a study that linked more B6 to less colon CA. Yet on April 28th, I reviewed a study [...]</p>
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