Vitamin MePA Testimonials
Prostate Cancer
Theory suggests that vitamin MePA might be effective against cancer. MePA is the antiaging vitamin. Cancer is mainly a disease of old age. Theory suggests that in the process of rolling back aging, the agingrelated disease of cancer might also be rolled back. Here is the first evidence that this theoretical expectation may be realized.
by Thomas James Godfrey; October 1, 2017
The last chapter in Aging: Cause and Cure, by Dr. Gerald E. Aardsma, covers a personal testimonial of his experience with taking methylphosphonic acid (MePA) as well as that of his wife. They are the first two people known to have begun testing this experimental vitamin in modern times. I am the third. This is my own testimonial, submitted at his invitation. He invited me to participate in a trial when he found out that I have a medical condition that might be improved by taking MePA. Let me begin with some background. I hope it is not too boring.
In November 2013, a PSA (Prostate Specific Antigen) test result (9.3) and a digital rectal exam suggested that I might have prostate cancer. Later tests and consultations with specialists at the Duke Cancer Center in Durham, NC, confirmed this diagnosis. In particular, three of four targeted needle core biopsies on the left side of my prostate gland yielded a report of prostatic adenocarcinoma (prostate cancer), one with a Gleason score of 8, two with 6. No cancer was detected in any of the four other core biopsies, including all three taken on the right side. The "high grade" cancer found in my prostate gland was considered too pervasive and too aggressive to advise watchful waiting or any option for targeted treatment of only specific parts of the gland.
Therefore, on April 17, 2014, a robotic radical prostatectomy was performed on me at Duke as recommended. In less technical terms, my entire prostate gland was removed at this time, along with seminal vesicles and some nearby groups of lymph nodes. A nervesparing technique was used on the right side but not on the left side. The procedure was somewhat complicated, partly because my prostate was stuck to the front of a rectal wall. After the surgery, the removed items were examined to see whether any cancerous tissue was cut. Any cancer found at a cut would have meant that some cancer had been left behind in my body. No problem was found, and the Gleason score was revised down to 7. This was all good news, suggesting that I might be rid of prostate cancer.
On July 31 [data point 1 on the graph] and again on October 15, 2014 [point 2], I went back to Duke to have my PSA level checked. Both of these times, it was reported to be less than 0.01, which was considered undetectable PSA. This was good news too, because if PSA had been detected so long after the surgery, it would probably mean that some cancer cells had escaped the prostate and continued to produce PSA somewhere else in my body.
Unfortunately, this was not the end of the story. The next test on March 27, 2015 [point 3], showed that the level was up to 0.04, but this was still too low to cause concern. Similarly, even though the result of yet another test on March 7, 2016 [point 4], was 0.25, not even this level seemed particularly alarming to me. However, when the result of a test on April 7, 2017 [point 5] was 1.6, I became concerned. In 2016 and again in 2017, the PSA level was about six times what it had been the year before. My doctor at Duke agreed that I should be concerned and recommended that I have the PSA test repeated at Duke. I had this done there on May 23 [point 6], and the result was 1.93, even higher than it had been the month before. (Results from different labs are not necessarily comparable.) At this visit to Duke, I also consulted with a radiation oncologist, who suggested that I was probably going to want to do something about this "biochemical recurrence" of prostate cancer. Cancerous cells had evidently escaped from my prostate before surgery after all. None of the suggested treatment options seemed pleasant to me.
PSA doubling time (how long it takes one's PSA level to double) is considered a measure of how aggressive the cancer is. If it is very slow, say a year or more, the problem might be ignored by someone my age (70 in June). I wanted to see a medical oncologist for a second opinion. Perhaps like many men, I considered hormone therapy and any form of castration, chemical or otherwise, to be obnoxious, an absolute last resort. I returned to Duke on June 16 for the desired second opinion of a highly qualified medical oncologist. We agreed to wait on beginning treatment, since my PSA was still rather low. He wanted me to come back for a bone scan and another PSA test in about three months to get a better handle on how aggressive my cancer is. He calculated my PSA doubling time then to be 4.9 months, which he considered indicative of fairly aggressive growth of the cancer.
Not long after the visit to Duke in June, I let Dr. Aardsma know about my condition, and he immediately suggested trying MePA to see whether it might help improve my condition. At first, I tried to buy MePA on the open market but discovered that it is sold to research organizations and educational institutions only. It could not be shipped to a private residence. Fortunately, Dr. Aardsma graciously supplied me with a dropper bottle of his vitamin MePA dietary supplement, and I started using it on July 17. For the first six days, my dose rate was 2 micrograms per day. Ever since then, with his assent, it has been 4 micrograms per day.
After I started taking MePA and while waiting for my September appointment at Duke, I was already in good health and did not notice any remarkable change in my health, with only one or two possible exceptions. When I went to see the solar eclipse in August, I got sunburned, and I was surprised that it did not hurt at all. I also suspect some improvement in healing time. I accidentally jabbed a sharp stick into the palm of my hand. Today, less than four weeks later, the wound is barely detectable as a faint scar.
The "acid test" of MePA came on September 27, when I returned to Duke for the bone scan and my most recent PSA test. (My bone scan raised no concerns, but this result was expected.) If my PSA doubling time had remained steady, then my PSA level would have been at about 2.5 when I started taking MePA, and it should have risen to about 3.5 by the date of this test. Those projected levels could have been even higher, depending on the data points selected for inclusion in the calculation of doubling time.
I was amazed by the new result, which was only 2.31, well below the expected level, even with a conservative doubling time.
Dr. Aardsma provided the chart above to illustrate. The black line plots my rising PSA level (either measured or extrapolated), the vertical red line marks the date of my first dose of MePA, and the pink dot at the right edge [point 7] marks my unexpected PSA test result (2.31). Each date at the bottom is 200 days before or after an adjacent date. Of course, PSA levels are indicated at the left edge. My oncologist was evidently less amazed than I was. He explained that the doubling time can vary when the PSA level is still this low, but we agreed that there was no need for me to begin treatments right away. He wanted me to come back for another PSA test and consultation in about three months.
Regardless of my doctor's expert opinion, I am delighted and thankful, not only to Dr. Aardsma but also to God and to those who prayed for me. After all, it was ultimately God who left us reliable life span data in Genesis and gifted Dr. Aardsma with the faith, patience, intelligence, determination, and whatever else may have been needed to take enough advantage of the information provided to discover vitamin MePA. Nevertheless, not even this matches God's wonderful grace and the gift of eternal salvation to me and anyone else who will receive it (John 3:16; Rev. 22:1617).
The latest PSA result suggests that my system has been significantly rejuvenated, allowing it to fight off cancer cells, wherever they may be in my body, especially in light of the fact that the level of MePA in my system, though slowly rising, may still be well below the optimum level. Of course, the results of my next PSA test, currently scheduled for early January, should be even more enlightening with regard to my future prospects for full recovery from prostate cancer. In the meantime, I am continuing to take MePA without any other form of cancer therapy.
If MePA can cure Dr. Aardsma's case of CIDP (Chronic Inflammatory Demyelinating Polyneuropathy) and my biochemical recurrence of prostate cancer, then it offers everyone with a similar medical condition considerable hope of dramatic improvements in health at low cost and in a short amount of time. Obviously, it would take hundreds of years to prove that MePA can allow someone to live to be hundreds of years old. Anyone waiting for this proof may wait too long and never receive any benefit, but MePA should still be attractive if it really does provide significant improvement in quality of life now. Please see Helen Aardsma's personal testimonial in Aging: Cause and Cure for a case where a significant health benefit has been noticed even though no serious medical condition was involved.
Anecdotal evidence like mine should be considered less reliable than formal clinical studies, of course, but at this stage, even this kind of evidence should be of interest. Not counting the fascinating theory behind Dr. Aardsma's discovery, this is still the best evidence of MePA effectiveness that can be offered at this time. As usual, your results may vary.
Closing Comment by Dr. Aardsma
Tom pointed out to me the following remarkable claim from a prostate cancer clinical trial (www.clinicaltrials.gov/ct2/show/NCT01763944) he declined to participate in because of his involvement with the vitamin MePA test.
No treatments have been shown to slow prostate cancer progression after radical prostatectomy.
This means that Dr. Aardsma's Vitamin MePA Dietary Supplement appears to be doing what no treatment has so far been able to do.
Update
Tom's PSA was measured again on January 3, 2018. The measured value was 3.44 ng/ml. This is higher than his previous PSA measurement of 2.31 ng/ml, but still only 62% of the 5.59 ng/ml predicted by the black, previtamin trendline shown in the graphs above. This result continues to support the hypothesis that vitamin MePA has slowed prostate cancer progression in Tom. The statistical basis for this conclusion follows.
by Gerald Aardsma; January 27, 2018
Because prostate cancer is an agingrelated disease, the theoretical expectation is that vitamin MePA—the antiaging vitamin—might be active against it. This gives rise to the following hypothesis pair.
 null hypothesis: Vitamin MePA has no impact on the progression of prostate cancer.
 alternate hypothesis: Vitamin MePA is active against prostate cancer.
A graph including the latest data point is shown below. Visual inspection of this graph suggests that the trend of the data points may be different after Tom began to use Dr. Aardsma's Vitamin MePA Dietary Supplement than it is before, implying a reduction in the rate of progression of the cancer. The objective of this study was to determine whether this visual impression was supported by a formal, quantitative statistical analysis.
Overview
Elementary biological theory expects prostate cancer progression after prostatectomy to be accurately described by a simple exponential growth curve.
Though the trend of Tom's data appears to change with the advent of inclusion of vitamin MePA in his diet, this might be explained as merely due to normal statistical fluctuations in the data points around an underlying simple exponential growth curve. In that case, the null hypothesis, that vitamin MePA has no impact on the progression of prostate cancer, would remain a possibility.
To test the null hypothesis, I first asked whether the previtamin data points could be described by a simple exponential growth curve. I used a standard weighted least squares analysis and found, not surprisingly, that they could.
I then asked whether the total set of eight data points could be described by a simple exponential growth curve, using the same weighted least squares analysis. A formal statistical analysis found that the likelihood that a simple growth curve properly describes these eight data points is roughly 1 in 8. Thus, the null hypothesis was tentatively rejected with a level of significance of 0.125 and the alternate hypothesis—that Vitamin MePA is active against prostate cancer—was tentatively accepted.
Details
Simple exponential growth has the mathematical form C = C_{0} e^{t/τ}. In the present case, C is the number of cancer cells at time t, beginning with C_{0} cells at t = 0. The constant, τ, controls how quickly the population of cells increases.
Meaningful application of this equation to the present dataset via a least squares analysis requires that the data points be appropriately weighted [Bevington 1969, 168]. It is not sufficient to weight the data points based on their analytical uncertainty alone, as analytical variability in total PSA (tPSA) is minor relative to biological variability [Nixon et al. 1997]. Total variability, which includes both analytical variability and biological variability, is needed for weighting the data.
The total coefficient of variation, CV_{t}, is defined as the standard deviation divided by the mean.[ Bunting et al. [2002] found an intraindividual CV_{t} of 21.6% for tPSA of a cohort of men with prostate cancer. This was for a oneyear time interval, but Bunting et al. reported that CV_{t} was "not greatly affected by the time window for measurements in the interval of 6 months to 2.7 years" [Bunting et al. 2002, 471]. The weights assigned in the present analysis used the Bunting et al. value for CV_{t}. Specifically, the standard deviations of the data points were calculated as σ_{i} = tPSA_{i} × CV_{t} = 0.216 tPSA_{i}, and the inverse squares of these standard deviations were used as weights in accordance with standard practice.
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The first two data points were exceptions to this otherwise uniform treatment. They were reported as 0.005 ng tPSA/ml. This appears to be at, or very near to, the analytical limit of detection, and to be significantly below a reasonable biological limit of detection for tPSA [Junker et al., 1999]. If σ_{i} = 0.216 tPSA_{i} is used for these two points, then their computed standard deviations are unreasonably small (0.001 ng/ml). This exaggerated precision exaggerates the influence of these first two points on the final fitted growth curve. To avoid this problem, the standard deviation of the third data point was assigned to the first two points as well. This gives these first three points equal weight in determination of the final least squares fit curve. This procedure seems a reasonable approximation since the third data point is still quite small, but clearly above the analytical detection limit.
The dataset is summarized in the following table.
Point Number  Days from Prostatectomy  tPSA (ng/ml)  σ 
1  105  0.005  0.00864 
2  181  0.005  0.00864 
3  344  0.040  0.00864 
4  690  0.250  0.05400 
5  1086  1.600  0.34560 
6  1132  1.930  0.41688 
7  1259  2.31  0.49896 
8  1357  3.44  0.74304 
Least squares application of a simple exponential growth curve to this dataset was facilitated by linearization of the growth curve equation via its logarithmic form, ln(N) = t/τ + ln(C_{0}), in accordance with standard practice [Bevington 1969, 180–185]. A spread sheet was then sufficient to carry out the needed least squares computations.
Results
The fit to the first six data points is shown below. For this exponential growth curve, PSA_{0} = (7.36±2.12)×10^{3} ng/ml and τ = 202±13 days. The goodnessoffit statistic, reduced chisquare, was 0.819, indicating a reasonable fit [Bevington 1969, 190 and Table C4].
The final figure shows the result of the least squares fit to the total dataset. This exponential growth curve gave PSA_{0} = (9.81±2.51)×10^{3} ng/ml and τ = 223±12 days. The goodnessoffit statistic in this case was 1.68, indicating a bad fit [Bevington 1969, 190 and Table C4].
Conclusions
Dr. Aardsma's Vitamin MePA Dietary Supplement appears possibly to have slowed the progression of prostate cancer following prostatectomy.
A formal clinical trial to check the result of this singleparticipant pilot study is required.
Acknowledgments
I would like to thank Tom Godfrey for providing the data and for helpful discussions regarding it. I would also like to thank my son, Matthew, for his assistance in bringing to light several journal articles used in this study. Thanks are due also to both Tom and Matthew for reviewing the article prior to its publication.
References
 Bevington, P.R. Data Reduction and Error Analysis for the Physical Sciences (New York: McGrawHill Book Company, 1969).
 Bunting, P.S., DeBoer, G., Choo, R., Danjoux, C., Klotz, L., and Fleshner, N. "Intraindividual variation of PSA, free PSA and complexed PSA in a cohort of patients with prostate cancer managed with watchful observation" Clinical Biochemistry (September 2002) Volume 35, Issue 6, 471–475.
 Junker, R., Brandt, B., Semjonow, A., Erren, M., Zechel, C., Assmann, G. "The biologic lower detection limit of six ultrasensitive PSA assays" Anticancer Res. (1999 Jul–Aug) 19(4A), 2625–8.
 Nixon, R.G., Wener, M.H., Smith, K.M., Parson, R.E., Blase, A.B., and Brawer, M.K. "Day to day changes in free and total PSA: significance of biological variation" Prostate Cancer and Prostatic Diseases (1997) 1, 90–96.
April 7, 2018 Update
Two more measurements have been added since the last update. These are shown in the table and the graph below. These latest two data points add further support for the hypothesis that vitamin MePA has slowed progression of this prostate cancer.
Point Number  Days from Prostatectomy  tPSA (ng/ml)  σ 
1  105  0.005  0.00864 
2  181  0.005  0.00864 
3  344  0.040  0.00864 
4  690  0.250  0.05400 
5  1086  1.600  0.34560 
6  1132  1.930  0.41688 
7  1259  2.31  0.49896 
8  1357  3.44  0.74304 
9  1420  4.25  0.91800 
10  1447  4.43  0.95688 
Error bars (1σ) have been added to the graph to help visualize the scatter in the data points.
Statistical analysis with the new data included strengthens acceptance of the alternate hypothesis that Vitamin MePA is active against prostate cancer. The null hypothesis may now be rejected with a level of significance of 0.088. The probability that rejection of the null hypothesis is the wrong choice reduces from 1 in 8 to 1 in 11.
Not only the bad fit of the simple exponential growth curve to these ten data points, but also the distribution of the data points about the fitted line argues for rejection of the null hypothesis. The three points preceding start of MePA supplementation all lie above the fitted exponential line, while the four points after MePA supplementation begins all lie below the fitted line. The probability of this happening by chance is 1 in 128 (less than 1%).
