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How much of this is due to government advice on food and therapy?
The WHO-EU-Monica study where fat and fruit&veg were negatively associated with CHD deaths while carbohydrate (estimated by subtraction) was positively associated with CHD deaths. Calculations based on the data in reports(European cardiovascular disease statistics, 2000, 2005, 2008, 2013 ). Data from the 2005 report for the following regression analyses:
Total Fat v. CHD deaths
Total Fat Multiple R = 0.668; R2 = 0.446; p = 5.43E -07
FAT% Coefficients Standard Error t Statistic P-value Lower 95.00 Upper 95.00
Intercept 929.335 97.124 9.569 <0.0001 733.332 1125.339
x1 -19.205 3.090 -6.214 <0.0001 -25.442 -12.968
Carbohydrates v. CHD deaths
EU countries relationship between carbohydrates and CHD incidence.
Multiple R = 0.667; R2 = 0.446 p = 2.58E-9
Carbs Coefficients Standard Error t Statistic P-value Lower 95.00 Upper 95.00
Intercept 929.335 97.124 9.569 <0.0001 733.332 1125.339
x1 -19.205 3.090 -6.214 <0.0001 -25.442 -12.968
Fruit%Veg v. CHD
EU countries relationship between Fruit&Veg and CHD incidence.
Multiple R = 0.591; R2 = 0.349 p < 0.0001
F&V Coefficients Standard Error t Statistic P-value Lower 95.00 Upper 95.00 Intercept 6.834 0.359 19.048 <0.0001 6.110 7.558
x1 -0.004 0.001 -4.746 <0.0001 -0.006 -0.002
This analysis of fat intake and Coronary Heart Disease (CHD) was based on data taken from the European Cardiovascular Statistics for1998-1999 (http://www.ehnheart.org/files/statistics 2005 ). The national data was tabulated (country, fat intake %age of diet {as energy} and CHD rate) and then sorted on fat intake (total or saturated) and then plotted with fat% (total or saturated) on the x-axis. Carbs %ages were obtained by subtraction. There were four reports; 2000 (a preliminary report) followed by reports in 2005, 2008 and 2013( this last report excluded saturated fat)
In short, the greater the national carb intake, the higher the national incidence of CHD. Conversely, the greater the national fat intake, the lower the national incidence of CHD.
Next take a look at the report of the NHBLI/CDC announcing the epidemic of CHF (Congestive Heart Failure) and its apparent association with increased use of statins.
This was rapidly removed from both websites. When questioned as to the reason removing this “epidemic” there was no response. The original NHBLI claim on this matter can be found on https://wayback.archive-it.org/3635/20130901052131/http://library.thinkquest.org/27533/facts.html. There remains a serious question as to why this fact sheet was removed - no answe from the CDC.
CHF is clearly rising with the increasing attempts to lower cholesterol. 1987 was about the time of statin introduction. The CHF epidemic is still extant and rising but the possibility of this increase is simply ignored.
Then there is the WHO-BHF graph for TC (total cholesterol) levels and surivial.
Estimated lowest mortality rates for TC blood levels
All Cause mortality 222 mg/dl 5.75 mmol/L
Non-communicable disease 210 mg/dl 5.49 mmol/L
Cardiac Disease 208 mg/dl 5.44 mmol/L
http://www.heartstats.org/documents/download.asp?nodeib=6797 This URL no longer exists? WHY?
Now on https://renegadewellness.files.wordpress.com/2011/02/cholesterol-mortality-chart.pdf
http://healthcorrelator.blogspot.co.uk/2009/12/total-cholesterol-and-cardiovascular.html
Again why was this removed around the time of the spat between the BMJ and Collins - no answer when questioned,
Now to Alzheimer’s Disease (AD)
Lorin’s book “Alzheimer’s Solved” a review with some 3,000 references is simply ignored.
AD/PD 2009 - Are We Experiencing an Alzheimer's Epidemic? Incidence Has Soared Enormously http://www.medscape.com/viewarticle/590106
March 25 , 2009 (Prague, Czech Republic) — The world may be experiencing an epidemic of Alzheimer's disease (AD ) that is not entirely attributable to an aging population, new research suggests. Presented here at AD/PD 2009: 9th International Conference on Alzheimer's and Parkinson's Diseases,
Murray Waldman, MD, from St. John's Rehabilitation Hospital, in Toronto, Ontario, found that while citations in the medical literature for femur fractures rose from 1706 to 3730 between 1996 and 2000, citations for AD and other dementias shot up from 1274 to 21 569 during the same time period. 1996 is relatively recent.
To quote Dr Waldman: “Epidemiological da ta collected over a 25-year period shows the incidence of AD in the 1960s was 2% in people over the age of 85 years, whereas today, most experts accept that the incidence of AD in this population is 50%. It is 20% over the age of 75 years and 10% in individuals over the age of 65 years”
Then consider diet where the development of Type 3 diabetes and its relationship to Alzheimer’s[1] and the association of a high carbohydrate diet with Alzheimer’s (Seneff[2]). These studies seem to be ignored while claims of low cholesterol and statin benefit in short term studies. The Solomon papers([3][4] that propose high cholesterol as contributing factor in Alzheimer’s but they completely ignore the therapy that invariably follows high cholesterol. However the summary in paper [3] the following comment occurs: “Serum TC levels decreased in most individuals................”but decreasing serum TC after midlife may reflect ongoing disease processes and may represent a risk marker for late-life cognitive impairment. The earlier paper [4] is more interesting in that it provides numbers while ignoring the therapy details by stating that they were N/A (not available). No therapy details in medical records; really! This a clear case of deliberate obfuscation.
On the basis of the data provided in the Solomon study I formed the following hypothesis:
My hypothesis is that long term statin use and low cholesterol has no effect nor protects against AD as is suggested by some studies.
H0 = No effect or protection: p > 0.05
H1 = NO protection or increases incidence: p < 0.05 Reject H0
Desirable suggests that <200 mg/dl requires no lowering of TC levels.
Borderline suggests that in the range 200–239 mg/dl some lowering might be required under official US guidelines
High implies that in the range ≥240 mg/dl immediate therapy with cholesterol lowering drugs.
Given the US paranoia over cholesterol, replacing row titles in Tables 2-4 with the US guideline treatment advice over 2-3 decades is reasonable and gives a very different picture;
namely that long term cholesterol lowering therapy can and does result in neurological damage. Incidentally, in both Solomon papers cited there is no mention of therapy
It therefore seemed reasonable to re-analyse the data in Table 2 with this long term use of statins (80+% of patients are tolerant to statins so that fear would result in long term use).
Table 2 in the 2009 Solomon paper provides the details (unfortunately there is no way of introducing tables in rapid responses
Extracting Desirable (<200 mg/dl) data for No AD and AD and (>239 mg/dl) provides the numbers for an OR analysis
I give the results of my analyses below:
Add in therapy based on US guidelines for the cholesterol levels and the results look rather different
Odds Ratio Confidence Interval Calculation For 2x2 Contingency Table
Solomon A. et al report Dement Geriatr Cogn Disord 2009;28:75–80
No dementia AD Total
NO TREAT (<200 mg/dl) 2545 107 2652
STATINS (≥240 mg/dl) 2932 176 3108
Total 5477 283 5760
Result 1.403529
Real Difference = 1.60%
Odds ratio = 1.43 = 43% relative rate(RR) increase in AD from treated high TC
Inflation of effect by using RR over real rate = 25.22 or 25-fold
95% confidence interval from 1.12 to1.83
Chi-square with Yates correction
Chi squared equals 7.775 with 1 degrees of freedom.
The two-tailed P value equals 0.0053
While experts are saying that it’s difficult to pinpoint “one particular cause” as the reason, it’s still absolutely shocking that we haven’t made more progress in establishing the factors that are associated with these diseases rather than concentrating on therapy— especially since most of Big Pharma’s focus is on creating wildly expensive drugs for these conditions.
From my position, things started going wrong in the 1960-70s with the advent of the “food plates/pyramids”. Obesity, metabolic syndrome, diabetes, insulin resistance, the “cholesterol hypothesis”, Alzheimer’s etc. For example the MHRA DAPs for simvastatin and atorvastatin show that nearly 50% of individual reports include the categories "Nervous system disorders" and "Psychiatric disorders" (Golomb[5]) yet this is simply ignored by the mainstream research. This all reminds me as a re-run of the tobacco companies agnotological defence of their industrial profit.
2. S. Seneff et al. / European Journal of Internal Medicine 22 (2011) 134–140 Nutrition and Alzheimer's disease: The detrimental role of a high carbohydrate diet
3 Solomon, A. et al Neurology. 2013 Mar 6;68(10):751-6.
Solomon Serum cholesterol changes after midlife and late-life cognition - twenty-one-year follow-up study.
4. Solomon, A. et al Dement Geriatr Cogn Disord 2009;28:75–80 DOI: 10.1159/000231980
Midlife Serum Cholesterol and Increased Risk of Alzheimer’s and Vascular Dementia Three Decades Later
5. Golomb, BA et al Statin Adverse Effects: ..... Am J Cardiovasc Drugs. 2008 ; 8(6): 373–418.
Re: Tick tock, how long have I got?
How much of this is due to government advice on food and therapy?
The WHO-EU-Monica study where fat and fruit&veg were negatively associated with CHD deaths while carbohydrate (estimated by subtraction) was positively associated with CHD deaths. Calculations based on the data in reports(European cardiovascular disease statistics, 2000, 2005, 2008, 2013 ). Data from the 2005 report for the following regression analyses:
Total Fat v. CHD deaths
Total Fat Multiple R = 0.668; R2 = 0.446; p = 5.43E -07
FAT% Coefficients Standard Error t Statistic P-value Lower 95.00 Upper 95.00
Intercept 929.335 97.124 9.569 <0.0001 733.332 1125.339
x1 -19.205 3.090 -6.214 <0.0001 -25.442 -12.968
Carbohydrates v. CHD deaths
EU countries relationship between carbohydrates and CHD incidence.
Multiple R = 0.667; R2 = 0.446 p = 2.58E-9
Carbs Coefficients Standard Error t Statistic P-value Lower 95.00 Upper 95.00
Intercept 929.335 97.124 9.569 <0.0001 733.332 1125.339
x1 -19.205 3.090 -6.214 <0.0001 -25.442 -12.968
Fruit%Veg v. CHD
EU countries relationship between Fruit&Veg and CHD incidence.
Multiple R = 0.591; R2 = 0.349 p < 0.0001
F&V Coefficients Standard Error t Statistic P-value Lower 95.00 Upper 95.00 Intercept 6.834 0.359 19.048 <0.0001 6.110 7.558
x1 -0.004 0.001 -4.746 <0.0001 -0.006 -0.002
This analysis of fat intake and Coronary Heart Disease (CHD) was based on data taken from the European Cardiovascular Statistics for1998-1999 (http://www.ehnheart.org/files/statistics 2005 ). The national data was tabulated (country, fat intake %age of diet {as energy} and CHD rate) and then sorted on fat intake (total or saturated) and then plotted with fat% (total or saturated) on the x-axis. Carbs %ages were obtained by subtraction. There were four reports; 2000 (a preliminary report) followed by reports in 2005, 2008 and 2013( this last report excluded saturated fat)
In short, the greater the national carb intake, the higher the national incidence of CHD. Conversely, the greater the national fat intake, the lower the national incidence of CHD.
Next take a look at the report of the NHBLI/CDC announcing the epidemic of CHF (Congestive Heart Failure) and its apparent association with increased use of statins.
This was rapidly removed from both websites. When questioned as to the reason removing this “epidemic” there was no response. The original NHBLI claim on this matter can be found on https://wayback.archive-it.org/3635/20130901052131/http://library.thinkquest.org/27533/facts.html. There remains a serious question as to why this fact sheet was removed - no answe from the CDC.
CHF is clearly rising with the increasing attempts to lower cholesterol. 1987 was about the time of statin introduction. The CHF epidemic is still extant and rising but the possibility of this increase is simply ignored.
Then there is the WHO-BHF graph for TC (total cholesterol) levels and surivial.
Estimated lowest mortality rates for TC blood levels
All Cause mortality 222 mg/dl 5.75 mmol/L
Non-communicable disease 210 mg/dl 5.49 mmol/L
Cardiac Disease 208 mg/dl 5.44 mmol/L
http://www.heartstats.org/documents/download.asp?nodeib=6797 This URL no longer exists? WHY?
Now on https://renegadewellness.files.wordpress.com/2011/02/cholesterol-mortality-chart.pdf
http://healthcorrelator.blogspot.co.uk/2009/12/total-cholesterol-and-cardiovascular.html
Again why was this removed around the time of the spat between the BMJ and Collins - no answer when questioned,
Now to Alzheimer’s Disease (AD)
Lorin’s book “Alzheimer’s Solved” a review with some 3,000 references is simply ignored.
AD/PD 2009 - Are We Experiencing an Alzheimer's Epidemic? Incidence Has Soared Enormously http://www.medscape.com/viewarticle/590106
March 25 , 2009 (Prague, Czech Republic) — The world may be experiencing an epidemic of Alzheimer's disease (AD ) that is not entirely attributable to an aging population, new research suggests. Presented here at AD/PD 2009: 9th International Conference on Alzheimer's and Parkinson's Diseases,
Murray Waldman, MD, from St. John's Rehabilitation Hospital, in Toronto, Ontario, found that while citations in the medical literature for femur fractures rose from 1706 to 3730 between 1996 and 2000, citations for AD and other dementias shot up from 1274 to 21 569 during the same time period. 1996 is relatively recent.
To quote Dr Waldman: “Epidemiological da ta collected over a 25-year period shows the incidence of AD in the 1960s was 2% in people over the age of 85 years, whereas today, most experts accept that the incidence of AD in this population is 50%. It is 20% over the age of 75 years and 10% in individuals over the age of 65 years”
Then consider diet where the development of Type 3 diabetes and its relationship to Alzheimer’s[1] and the association of a high carbohydrate diet with Alzheimer’s (Seneff[2]). These studies seem to be ignored while claims of low cholesterol and statin benefit in short term studies. The Solomon papers([3][4] that propose high cholesterol as contributing factor in Alzheimer’s but they completely ignore the therapy that invariably follows high cholesterol. However the summary in paper [3] the following comment occurs: “Serum TC levels decreased in most individuals................”but decreasing serum TC after midlife may reflect ongoing disease processes and may represent a risk marker for late-life cognitive impairment. The earlier paper [4] is more interesting in that it provides numbers while ignoring the therapy details by stating that they were N/A (not available). No therapy details in medical records; really! This a clear case of deliberate obfuscation.
On the basis of the data provided in the Solomon study I formed the following hypothesis:
My hypothesis is that long term statin use and low cholesterol has no effect nor protects against AD as is suggested by some studies.
H0 = No effect or protection: p > 0.05
H1 = NO protection or increases incidence: p < 0.05 Reject H0
categories: Cholesterol categories
Desirable (<200 mg/dl)
Borderline (200–239 mg/dl)
High (≥240 mg/dl)
Desirable suggests that <200 mg/dl requires no lowering of TC levels.
Borderline suggests that in the range 200–239 mg/dl some lowering might be required under official US guidelines
High implies that in the range ≥240 mg/dl immediate therapy with cholesterol lowering drugs.
Given the US paranoia over cholesterol, replacing row titles in Tables 2-4 with the US guideline treatment advice over 2-3 decades is reasonable and gives a very different picture;
namely that long term cholesterol lowering therapy can and does result in neurological damage. Incidentally, in both Solomon papers cited there is no mention of therapy
It therefore seemed reasonable to re-analyse the data in Table 2 with this long term use of statins (80+% of patients are tolerant to statins so that fear would result in long term use).
Table 2 in the 2009 Solomon paper provides the details (unfortunately there is no way of introducing tables in rapid responses
Extracting Desirable (<200 mg/dl) data for No AD and AD and (>239 mg/dl) provides the numbers for an OR analysis
I give the results of my analyses below:
Add in therapy based on US guidelines for the cholesterol levels and the results look rather different
Odds Ratio Confidence Interval Calculation For 2x2 Contingency Table
Solomon A. et al report Dement Geriatr Cogn Disord 2009;28:75–80
No dementia AD Total
NO TREAT (<200 mg/dl) 2545 107 2652
STATINS (≥240 mg/dl) 2932 176 3108
Total 5477 283 5760
Result 1.403529
Real Difference = 1.60%
Odds ratio = 1.43 = 43% relative rate(RR) increase in AD from treated high TC
Inflation of effect by using RR over real rate = 25.22 or 25-fold
95% confidence interval from 1.12 to1.83
Chi-square with Yates correction
Chi squared equals 7.775 with 1 degrees of freedom.
The two-tailed P value equals 0.0053
According to a recent news item Alzheimer’s is now the top cause of death in the England and Wales. I would add that dementia is a condition that is most likely to be noticed within the family circle first. (https://www.theguardian.com/society/2016/nov/14/dementia-and-alzheimers-... )
While experts are saying that it’s difficult to pinpoint “one particular cause” as the reason, it’s still absolutely shocking that we haven’t made more progress in establishing the factors that are associated with these diseases rather than concentrating on therapy— especially since most of Big Pharma’s focus is on creating wildly expensive drugs for these conditions.
From my position, things started going wrong in the 1960-70s with the advent of the “food plates/pyramids”. Obesity, metabolic syndrome, diabetes, insulin resistance, the “cholesterol hypothesis”, Alzheimer’s etc. For example the MHRA DAPs for simvastatin and atorvastatin show that nearly 50% of individual reports include the categories "Nervous system disorders" and "Psychiatric disorders" (Golomb[5]) yet this is simply ignored by the mainstream research. This all reminds me as a re-run of the tobacco companies agnotological defence of their industrial profit.
References
1. Journal of Diabetes Science and Technology Volume 2, Issue 6, November 2008 © Diabetes Technology Society”Alzheimer’s Disease Is Type 3 Diabetes—Evidence Reviewed
Suzanne M. de la Monte, M.D., M.P.H.1–3 and Jack R. Wands, M.D.3
2. S. Seneff et al. / European Journal of Internal Medicine 22 (2011) 134–140 Nutrition and Alzheimer's disease: The detrimental role of a high carbohydrate diet
3 Solomon, A. et al Neurology. 2013 Mar 6;68(10):751-6.
Solomon Serum cholesterol changes after midlife and late-life cognition - twenty-one-year follow-up study.
4. Solomon, A. et al Dement Geriatr Cogn Disord 2009;28:75–80 DOI: 10.1159/000231980
Midlife Serum Cholesterol and Increased Risk of Alzheimer’s and Vascular Dementia Three Decades Later
5. Golomb, BA et al Statin Adverse Effects: ..... Am J Cardiovasc Drugs. 2008 ; 8(6): 373–418.
Competing interests: No competing interests