Friday, 14 August 2015

Patients experiencing biochemical failure after prostatectomy for prostate cancer, often receive salvage radiation therapy

Patients experiencing biochemical failure — defined as an increase in prostate-specific antigen (PSA) level — after prostatectomy for prostate cancer often receive salvage radiation therapy (SRT) to control the disease and prevent metastases.
However, despite SRT, some patients still exhibit biochemical failure. Now, a long-term, single-center study, published online July 9 in the American Journal of Clinical Oncology, has demonstrated that outcomes for 61 men who experienced a biochemical recurrence after surgery, including a subset of 34 men who experienced failure twice (once after surgery and once after SRT), are robust.
The median overall survival was 13.6 years for the men in the study who had two biochemical recurrences and 14.7 years for the men who had just the one recurrence after surgery, report the authors, led by D. Nathan Kim, MD, PhD, from Texas Oncology in Waco.
Furthermore, the 10-year prostate-cancer-specific, metastasis-free, and castration-resistant-free survival (from the time of PSA failure after SRT) rates were all in excess of 70% for the men who had two biochemical recurrences.
The new retrospective data might be of service to clinicians in discussions with anxious patients because there is a "paucity" of prospective data about this clinical scenario, the authors suggest.
The extensive follow-up period makes the study one of the longest in the literature. Median follow-up was 126 months after SRT and 112 months after SRT failure. Most studies have a median follow-up of less than 90 months after SRT.
"Because of our long-term follow-up, we were able to make observations in those patients who recurred despite SRT," the authors write.
Although their study was of a single group of men, and thus not comparative in any way, the authors observe that another study on natural history after PSA failure demonstrated that the median time to distant metastasis was 8 years after PSA failure after radical prostatectomy (without SRT), and roughly one in three patients developed distant metastases within 5 years without radiation therapy.
"In our series, distant metastases-free survival at 5 years was 94% for all patients, and was 75% for those who failed after SRT," the authors report.
"The study suggests that SRT is effective in preventing prostate-cancer-specific mortality and decreases the rate of distant metastases," the team writes.
The new study also raises the issue of the timing of radiation therapy after prostatectomy.
Patients with pathologic T3 disease or positive margins are candidates for postoperative radiation therapy, said Colleen A.F. Lawton, MD, past chair of the American Society for Radiation Oncology (ASTRO) board of directors, who was not involved in the study.
This recommendation is based on the American Urological Association/ASTRO guidelines on the use of adjuvant and SRT after prostatectomy, which is endorsed by the American Society of Clinical Oncology (Int J Radiat Oncol Biol Phys. 2013;86:822-828).
PSA levels determine what's next for these patients, Dr Lawton told Medscape Medical News.
Patients with adverse pathologic features, such as seminal vesicle invasion, positive surgical margins, and extraprostatic extension without evidence of disease recurrence (i.e., undetectable PSA levels), are candidates for adjuvant radiation therapy (ART), said Dr Lawton, who is from the Medical College of Wisconsin in Milwaukee.
Patients who show increases in PSA at any time after surgery are candidates for SRT, she explained.
Patients with pathologic T3a disease should see a radiation oncologist and discuss whether they are candidates for ART or SRT, Dr Lawton said. "The issue is that many patients do not consult with their radiation oncologist," she told Medscape Medical News.
The new study findings do not challenge the guidelines, she suggested.

The study provides food for thought, but is not practice-changing.

"The study provides food for thought, but is not practice-changing," said Dr Lawton.
Nevertheless, in this study, the authors indicated that 70% of their patients would have been candidates for ART based on their pathologic stage and margin status. They emphasize that "without concrete evidence from randomized clinical trials, one must seriously consider the advantages and disadvantages of ART versus SRT."

"The decision of whether to use ART or SRT remains an area of active debate, and prospective randomized trials are currently underway to attempt to answer this question," they add.
The authors were referring to the RAVES trial (NCT00860652), which is a phase 3 study investigating the timing of radiation therapy for prostate cancer with high-risk features.
Active surveillance is indicated for men with a PSA level of 10 ng/L or less, a Gleason score below 6, and a pathologic disease stage of T2a or less, said Dr Lawton. She explained that if patients have pathologic T3 disease and undetectable PSA, other factors should be taken into account when deciding on management, including the presence of comorbidities.
Study Details
The analysis involved 61 men treated at the University of Texas Southwestern Medical Center in Dallas from 1992 to 2000 who underwent SRT following biochemical recurrence after prostatectomy.

Biochemical recurrence of the disease after surgery was defined as a persistently detectable PSA level of at least 0.05 ng/mL or two consecutive PSA increases of at least 0.1 ng/mL that triggered initiation of SRT.
Failure of SRT was defined as a single increase in PSA of at least 2 ng/mL from nadir levels, two consecutive PSA increases of at least 0.2 ng/mL, initiation of salvage treatment, or clinical disease recurrence.
At 10 years, overall survival was 67%, freedom from PSA failure was 33%, prostate-cancer-specific survival was 84%, and distant metastases-free survival was 84% for the men who failed SRT.

Pathologic T-stage, Gleason score, seminal vesicle involvement, and pre-SRT PSA were associated with freedom from PSA failure.
For patients who failed SRT, the median time to biochemical recurrence after SRT was 30 months.
A total of 19 patients (68%) received androgen-deprivation therapy.
Early SRT failure correlated with a significant decrease in distant metastases-free survival and prostate-cancer-specific survival. Ten-year distant metastases-free survival from SRT was 43% (recurrence at 1 year or sooner) versus 91% (recurrence at 1 year or beyond).

The study begs the question of whether biochemical failure is an important surrogate for clinical care in prostate cancer. Dr Lawton indicated that it is an important surrogate; however, there is no absolute proof about its being associated with survival.
Am J Clin Oncol. Published online July 9, 2015.

Sunday, 26 July 2015

Everything anything...


Great to find this link on the Internet, to a blog I had not yet seen. 
It gives such great support to the campaign back 5 years ago.
Wish we could do it all again!

 CLICK HERE

Wednesday, 15 July 2015

Graduation at Carlisle Cathedral...

Please excuse the self indulgence, but this was one of the proudest moments of my life. When I look at the boxes of work produced over those 4 years, it filled my car. It was a slog! I met some amazing people and had experiences that were beyond imagination. I had cancer surgery in first year, then smuggled a 4x4 into Serbia in my second. My third year fades from memory, unlike my fourth, in Johannesburg, which changed my life and will stay precious to me always. Without the support of my wonderful wife Beverley, it would have been impossible. In Carlisle Cathedral today, I couldn't help but feel a bit special. Daniel Sencier BA hons. I like it! Now I need to think about a career!   

Wednesday, 1 July 2015

Pioneering treatment at the Royal Surrey County Hospital...

                    Professor Stephen Langley, Donna Higgins, Claire Deering and John Cummins
Royal Surrey County Hospital has hit a significant milestone in the use of a prostate cancer treatment which has fewer side effects than surgery. 
Former GP John Cummins was the 3,000th patient to undergo brachytherapy treatment at the Guildford hospital last Thursday (June, 25). 
The technique uses small radioactive seeds, the size of a grain of rice, which are implanted into the prostate.
The procedure is said to have a 90% success rate in treating the cancer in its early stages – similar to radical surgery.
However, its major benefit is that it damages less of the unaffected tissue surrounding the prostate, and is far less evasive than surgery.
Mr Cummins, who is 77-years-old and from Chichester, said the procedure was a significant advancement.
“Until this came in, the only radical treatment to eliminate cancer of the prostate was a radical surgery, which was a pretty big undertaking,” he said. “Guildford appears to be the leading light.”
Mr Cummins was diagnosed with prostate cancer a couple of months ago, and was suitable for brachytherapy as a scan showed the cancer had not spread to other parts of his body.
He stressed the importance of seeing a doctor as soon as possible in order to get an early diagnosis.
Urologist Stephen Langley and oncologist Robert Laing first began treating patients in 1999 at the Royal Surrey’s St Luke’s Cancer Centre.
It is the largest centre offering this treatment in Europe and has been lauded as one of the top units in the world.
Prof Langley said: “Although there are some men who opt for robotic surgery which I regularly perform, most I believe are best suited to 4D brachytherapy.
“It offers the same chance of cure but with a fraction of the side effects.
“It is important that patients make a truly informed decision about their treatment options as the side effects can have a lasting impact on their lives.
“This approach uses a combination of seeds linked together around the outside of the prostate and loose seeds within the centre of the gland.
“A computer is used during the procedure to calculate the exact position of each seed.
“The implantation of the seeds, performed under a light general anaesthetic, takes 45 minutes and patients can return to normal life the following day, hence time, the fourth dimension, is optimised.
“The side effects of 4D brachytherapy have been shown to be significantly better than those patients treated with existing techniques.
“Brachytherapy is suitable for men whose cancer is confined to the prostate gland and who have few urinary symptoms such as a weak stream.”
Prof Langley and Dr Laing are trustees of the Prostate Project, a Guildford-based charity which raises money to help support people with the disease and funds treatments to tackle it.
One of the charity’s biggest drives has been raising £1.3 million for a new urology centre at the hospital.
Tim Sharp, a founding trustee of the Prostate Project, said: “We are very fortunate to have two such eminent clinicians as trustees, of the Prostate Project.
“Professor Langley is one of Europe’s leading Brachytherapy specialists. He has been instrumental in the creation of the new urology centre which will change forever how the urology patient is treated at the Royal Surrey.”

Thursday, 25 June 2015

When you're in the final hours of your life...


If you've ever danced with the Angel of Death, you'll know this to be true. 
If you never have, wake up before it's too late. 


Saturday, 20 June 2015

Killing Cancer Through the Immune System...

By Michael Howerton on February 04, 2014


One of the confounding characteristics of cancer has long been that the body’s usually active patrol against viruses tends to leave deadly cancer cells alone to fester, mutate and spread.



The immune system has this blind spot by design – an immune system that has an ability to attack itself leads to autoimmune diseases, so as protection, it screens out its own tissue.
T-cells (stained in pink and brown), which are used by the immune system to fight disease, show an increase near prostate cancer cells following an immunotherapy treatment. Image credit: Fong lab/UCSF


For decades, scientists assumed that cancer was beyond the reach of the body’s natural defenses. But after decades of skepticism that the immune system could be trained to root out and eliminate these malignant cells, a new generation of drugs is proving otherwise.
The treatment consists of infusing antibodies that enhance the immune system to recognize cancer cells and attack it. What’s more, since the immune system has a built-in memory, it continues to go after cancer cells, so the response can be longer lasting and more complete.
The trick is that this treatment doesn’t work for everybody, and researchers don’t yet understand why. But when it does work, the results have been particularly impressive.
“Although there is a 30-year history of people and institutions trying to develop immunotherapy approaches to cancer, it has only been in the last 10 years that we’ve broken through and have been able to impact cancer using immunotherapy,” said Jeffrey Bluestone, PhD, executive vice chancellor and provost of UC San Francisco.
“I do think that we’re at an inflection point with immunotherapy,” he added. “It will be revolutionary and will impact how we approach cancer for years to come.”

The Last Hope

Patricia Hollowell, 80, was diagnosed with melanoma in April 2012.
She had three surgeries in quick succession in her hometown of Grand Junction, Colo., that removed the tumors from her head but didn’t prevent them from coming back and spreading quickly to her neck and lymph nodes.
Patricia Hollowell spends time with her daughter Teri and
grandson Cody. Photo by Cindy Chew
On the day she returned home from the hospital after the third surgery in June of that year, her husband had a massive stroke and died a week later.
“It was the summer from hell, it was like everything was over,” she recalled. “When my husband died and my cancer came back it was like the world was over, my world was over. It was just complete devastation.”
This was not Hollowell’s first bout with cancer, having survived breast and colon cancer 30 years ago. This time, after the failed surgeries and with her cancer spreading quickly, she figured her luck would run out.
Her doctors suggested her only hope might be to join a clinical trial involving new cancer immunotherapy drugs.
Hollowell moved to San Rafael, Calif., to be with her daughter and was accepted into a trial at UCSF under the direction of Adil Daud, MD, director of melanoma clinical research at the UCSF Helen Diller Comprehensive Cancer Center. She began a biweekly IV of an antibody that targets an immune inhibitor called PD-1 in June 2013.
“Within a month, my doctors could see the difference, and I am now tumor-free,” she said. “For me, it’s been an absolute miracle.”
Patricia Hollowell gets a hug from her grandson Cody, 3, at her daughter's home in
San Rafael, Calif. Photo by Cindy Chew
Daud said use of the PD-1 antibody has been “a game-changer for melanoma therapy.” Just a few years ago, about 10 percent of his patients saw their tumors shrink with immunotherapy treatment; today the response rate has improved to 30 to 50 percent. That’s compared to chemotherapy treatment, which has a 10 percent response rate and can be a short-lived solution.
Immunotherapy is “not a sure thing even now, but a positive response is becoming a lot more likely with [the antibody for] PD-1,” Daud said. “Hopefully it will become a building block, and we will add to it and go beyond a 50 percent response rate in the coming years.”
For Hollowell, twice-monthly trips to UCSF for treatment could soon end if her PET scan at the end of February shows no present tumors.
“I feel really good,” she said. “The only bad part is that I’m a little tired, so I rest during the day, but the good part is I’m alive.”

Treating the Patient Instead of the Disease

“For the longest time, people did not believe this was possible,” said Lawrence Fong, MD, associate professor of medicine at UCSF and one of the University’s lead investigators in the expanding use of immunotherapy.
Lawrence Fong, MD, and Jera Lewis, a staff research associate in Fong's lab, pull cryopreserved patient samples stored in a liquid nitrogen tank to assess for immune responses. Photo by Susan Merrell
Cell cultures containing growing tumor cell lines are stored in Fong's lab. Photo by Susan Merrell
Fong and Yafei Hou, MD, PhD, a specialist in the Fong Lab, discuss which treated patients they plan to assess for immune responses. Photo by Susan Merrell
“Now we can treat cancer by treating the patient instead of the disease,” he said. “That’s the biggest change. We can treat cancer without delivering chemotherapy or radiation to kill the cancer or performing surgery to get rid of the tumor.”
Researchers at UCSF and elsewhere have identified cell receptors, such as CTLA-4 and PD-1, which act as a brake on the immune system, limiting its response.
With the use of antibodies to inhibit these blockade receptors, allowing a more active and vigilant immune system, doctors have seen outstanding responses in patients with metastatic melanoma and lung cancer, both of which are almost always fatal with conventional treatments. Immunotherapy also has been successful in cancers of the bladder, prostate, kidney and bone marrow.
“This was a radical idea: that the body already possesses the ability to defeat cancer, and that medicine’s role was to find a way to allow the body to marshal the healing work it is naturally capable of,” Fong said. “We all believed it could work, but very few would have predicted the 180-degree change that we’ve seen over the last two years.”
Ever since James Allison, PhD, developed the first drug that increased survival for patients with metastatic melanoma while at UC Berkeley – an antibody against CTLA-4 called ipilimumab that was approved by the U.S. Food and Drug Administration in 2011 – it has been like a door has swung open.
In December, Allison – now chair of the University of Texas MD Anderson Cancer Center’s Immunology Department – won one of the 2014 Breakthrough Prize in Life Sciences for his groundbreaking discovery. Max Krummel, PhD, who co-developed ipilimumab while a graduate student in Allison's lab, is now a pathology professor at UCSF.
Indeed, the treatment has been a hot topic at recent cancer conferences and all top pharmaceutical companies are developing immunotherapy drug programs. Science magazine declared immunotherapy its top breakthrough of 2013.
Bluestone’s UCSF lab was the first to show that CTLA-4 can turn off the immune system’s T-cell attack when studying its application to organ transplants and autoimmune disease, a discovery that help paved the way for Allison’s application to cancer.
He pointed to the University’s continuing role in pushing the field ahead, including recent work in cell therapy, which uses stem cells taken from a patient, corrects the gene mutation that causes disease and returns the “gene-corrected” cells to the patient for therapy.
This work is part of UCSF’s commitment to precision medicine, which aims to harness the wealth of genomic, clinical and environmental data from patients to develop more effective and even preventive therapies for human diseases.
“It has been a sea change that has been transformational,” Bluestone said, “not only from the patient’s point of view, but also for our understanding of the relationship between cancer and the immune system and how to treat disease.”

Immunotherapy’s Unanswered Questions

For all its success and promise, researchers still are baffled as to why immunotherapy works for some cancer patients, but not others.
“We have immunotherapy patients who live a long time, and now we can start to figure out why,” he added. “This is exactly what we’re focusing on in the lab now.”
In Fong’s lab, where he often works with Eric Small, MD, deputy director of UCSF Helen Diller Family Comprehensive Cancer Center, his team is studying immune system activity in prostate cancer patients, trying to determine in which cases the immune response is activated and whether T-cells attack the cancer and why.
One of the most promising avenues is to combine immunotherapy treatments. Fong’s lab is now working on several studies regarding immunotherapy drugs, including a combination trial of sipueleucel-T and ipilimumab, which is scheduled to continue for the next couple of years.
For many aggressive, late-stage cancers, immunotherapy won’t replace traditional cancer treatments like chemotherapy, radiation and surgery, but it can be a complementary approach, said Lewis Lanier, PhD, chair of the UCSF Department of Microbiology and Immunology who collaborates with Fong on studying how cancer affects the immune system’s natural responses.
“Chemotherapy can reduce tumors by 95 percent, but if you have just one cell left, it can come back. So you can use [chemotherapy] to buy time, to really shrink the tumor if it’s far advanced, and then use the immune drugs,” Lanier said.
When Robert Bruce, of El Dorado Hills, Calif., was diagnosed in March 2011 with Stage IV melanoma, he already had tumors on his lungs, ribs and lymph nodes.
Robert Bruce meets with Adil Daud, MD, at UCSF Medical Center to discuss the
progress of his immunotherapy treatments as part of Daud's clinical trial of the
PD-1 antibody. Photo by Cindy Chew
Bruce said his cancer wasn’t a case of his body betraying him, but actually the reverse: “I betrayed my own body.”
“I was a type-A personality, always stressed, and stress – as we all know now – is one of the biggest inhibitors to a healthy immune system,” he said. “And, I’d always been one to go out to into the sun and tan. My daughter would say, ‘Daddy, put on sunscreen,’ and I would say, ‘No, it’s just skin cancer. If something happens, they could just cut it out.’ I was an idiot.”
By the time his wife noticed a nasty-looking mole on his back and persuaded him to show it to his doctor, the cancer had metastasized throughout his whole body.
Bruce endured a brutal round of biochemotherapy, a combination of traditional chemotherapy with immunotherapy. The treatment didn’t seem to make a difference, and the prognosis for most Stage IV patients is six to nine months.
Adil Daud, MD. Photo by Cindy Chew
He began reading about a new generation of promising immune response drugs and was accepted for Daud’s trial of the PD-1 antibody at UCSF.
“At eight weeks, I got my first scan, and it showed 20 to 30 percent reduction in my tumor load,” Bruce said. “After almost a year of bad, bad stuff with no good news ever, all of a sudden, they were shrinking.”
His muscles and bones ache and hurt from the treatment, but compared to the debilitating biochemotherapy, Bruce said, “this has been a piece of cake.”
Every two weeks he watches his tumors decrease, and now they are virtually nonexistent.
“I feel like a kid on Christmas morning,” he said. “I’m 60 years old, and I was already looking at what I was going to miss out on – the grandkids, all those kinds of things.
“I’ve prayed about this, and initially it wasn’t just for a cure, but I asked for peace and for hope. What any cancer patient asks for is really that hope, that if this drug doesn’t do it, maybe it will keep me here long enough to find the next drug that will.”

Saturday, 13 June 2015

Pill that could halt prostate cancer...

 by RORY CLEMENTS, Daily Mail 12th June 2015

A once-a-day pill has been approved in Britain for use in the early stages of prostate cancer following a massive trial that showed it could reduce the risk of the disease progressing in 42 per cent of men.

Prostate cancer is known to 'feed' on the male hormone testosterone, but Casodex, which is a hormone-based drug, 'starves' the cancer by preventing testosterone getting to it. It works on receptors in the cells.

In the trial, Casodex was used alongside standard treat-ments of surgical removal of the prostate, radiotherapy or merely careful watching of the disease's development, often slow.

Those on the drug fared far better than those on a dummy pill. Many men's biggest fear is that treatment for prostate cancer will make them impotent and kill their love life.

Casodex has a vital advantage over some other hormone treatments in that it significantly reduces the risk of impotence.

Whereas other drugs block production of testosterone, Casodex allows testosterone to remain in the blood stream, but it doesn't allow it to get to the cancer.

Some hormone treatments cut off the supply of testosterone completely and in effect amount to 'chemical castration'. The new study, the world's biggest-yet prostate cancer trial, followed the fortunes of over 8,000 men in 23 countries, including Britain.

Dr Heather Payne, consultant clinical oncologist at the Middlesex Hospital, London, says: 'Most men feel that to be actually doing something to prevent the cancer coming back actually makes you feel more positive.

'And you don't want to have a treatment that is going to make you feel so dreadful that you start wondering whether it's worth having the medication. But this drug is well tolerated and doesn't harm the quality of life.'

Casodex has been used for many years in treating advanced prostate cancer, but this is the first time it has been studied and approved for use in the early stages.

'Before, people would just have the surgery or radiotherapy,' says Dr Payne. 'In this study, they had the surgery or radiotherapy and were then randomly given either Casodex or a placebo to see if that would improve results over the surgery or radiotherapy alone - and the drug did.'

Not only did it stop the disease progressing in 42 per cent of men against those who took the placebo, it also prevented the cancer spreading to the bones in a third of the patients. When the cancer gets to the bones it can be extremely painful.

Widower Alec Taylor, 70, a retired English teacher of Primrose Hill, North London, discovered he had early prostate cancer in 1997 after seeing his GP for a checkup and agreed to go on the Casodex trial.

He learned last week that he was one of those taking the real pill rather than the placebo. He is presently clear of cancer.

He said: 'The bad news was that I had cancer - the good news was that the tumour was very small. My treatment started in January 1998. The radiotherapy went on for 32 sessions over six weeks. I thought I'd go potty.'

'Then they mentioned the Casodex trial and I was told I could go on it if I wanted. I thought it was for the benefit of science, so I agreed to it and stuck it for two years. The great difficulty was to remember to take the things, same time every day. I missed only four.'



Saturday, 30 May 2015

Going to live in Thailand for 3 years

Our 18 months in South Africa, we agree, was the most amazing time of our lives. Beverley and I visited all 10 provinces, and also toured in Zimbabwe, Mozambique, Zambia, Botswana, and Swaziland. You can go on holiday to these places, but living there and experiencing the people and culture for so long, was breathtaking.

Back in the UK now for a short while before the next great adventure, Thailand, and this time it's for 3 years! From Bangkok we can reach out to Australia, India and Japan in just 6 or 7 hours, but within a 1 to 2 hour flight are amazing countries such as Malaysia, Cambodia, Indonesia, Borneo, Burma, China, Vietnam and Singapore, just to name a few. Comparing Johannesburg to Bangkok is difficult, they both have millions of inhabitants and a wet season, but nothing else is the same. Where Jozi is around a mile above sea level, hot and very dry, Bangkok is at sea level, even hotter and extremely humid. Thailand is positively safe when compared to South Africa, but no harm in staying cautious when traveling anywhere abroad these days. When I get there, I'll give you a taste of what it's like.

Thailand has strict rules about criticising the government or royal family and it's not allowed in any way, any where, ever. You can end up in prison quickly, so as a blogger, I intend to stay completely respectful to Thai laws, customs and regulations. All my research indicates that the country is most welcoming and a cultural feast to outsiders. The cost of living is even cheaper than South Africa, but I'm told to buy my clothes and shoes in the UK because they don't cater for men my height.

After Thailand, what next? Well, who can plan ahead more than 3 years? 

Friday, 29 May 2015

To take statins or not?

When I had a routine health check-up eight years ago, my cholesterol was so high that the laboratory thought there had been a mistake. I had 9.3 millimoles of cholesterol in every litre of blood — almost twice the recommended maximum. 
It was quite a shock. The GP instantly prescribed statins, the cholesterol-lowering drugs that are supposed to prevent heart disease and strokes. For eight years, I faithfully popped my 20mg atorvastatin pills, without side effects. Then, one day last May, I stopped. It wasn’t a snap decision; after looking more closely at the research, I’d concluded that statins were not going to save me from a heart attack and that my cholesterol levels were all but irrelevant. 
When I informed my GP of my decision three months later, I wasn’t entirely honest. Rather than say I was sceptical about the drugs, I told my doctor I’d quit the statins because they were causing pain in my arm. 
He didn’t bat an eyelid. Evidence from the drug industry published this month – evidence I suspect was heavily reliant on data from the drug industry, as Dr James Le Fanu pointed out on these pages last week – may suggest that side effects are uncommon, but previous studies have found that one in five people on statins suffers adverse side effects, from muscle pain and diarrhoea to memory loss and blurred vision. 
The GP simply suggested I try another brand of statin. The sooner the better, he said, given that I’d already been off my prescription for three months. “Hang on,” I said. “Could you give me a blood test first?” When the results came back, he was amazed that my total blood cholesterol was lower than when I’d been on statins. After three months without the pills, it was 5.4mmol/l (5.4 millimoles per litre of blood) compared with 5.7 mmol/l a year earlier.  
The only major changes I’d made to my lifestyle since coming off statins were eliminating sugar (including alcohol and starchy foods such as bread) and eating more animal fat. Many experts now believe that sugar is emerging as a true villain in the heart-disease story; while after decades of demonisation, saturated fat has been acquitted of causing heart disease by a recent “meta” analysis of 70 studies by Cambridge University. 
Typically, I was eating red meat three or four times a week and enjoying butter, full-fat milk and plenty of eggs. You would have thought that after three months on a diet so high in saturated fat, my cholesterol would have shot back up to pre-statin levels — but no, it came down and has stayed down seven months on. Not only that, but my levels of LDL (so-called bad cholesterol) were also lower than when I’d been on statins, and my ratio of HDL (so-called good cholesterol) to LDL was under four for the first time, an excellent sign, according to medical wisdom. 
Not that I cared about any of this. 
Yes, it was the statins that originally reduced my cholesterol levels so dramatically. But so what? I believe that high cholesterol has been a scapegoat for too long. Yes, it may, in some circumstances, be an indicator of heart disease but there is no evidence of a causal link. In my view, high total blood cholesterol or high LDL levels no more cause heart attacks than paramedics cause car crashes, even though they are present at the scene. 
Just lowering cholesterol with drugs without sorting out the dietary and lifestyle factors that actually cause heart disease is nonsensical. Besides, there are plenty of other, more reliable indicators of heart-disease risk. What further astonished my GP was that on these indicators I was now apparently better off in other ways than when I’d been on statins. My blood pressure was down. For the first time in years, I was slimmer, especially around the belly. My triglycerides — a type of blood fat with a causal link to heart disease — were lower than at any time in the preceding eight years. My fasting blood glucose was at the optimum level, whereas a year earlier it had been too high. My total white blood count — a marker of inflammation — was lower. 
My blood test for a marker called glycated haemoglobin (A1c), high levels of which are associated with heart disease and overall mortality, were bang on normal. Finally, my level of c-reactive protein (CRP) — a protein that rises in response to inflammation — was extremely low. So, biochemically, I was in excellent shape, better than when I’d been on the statins. “Have you taken up running?” asked my bemused GP. 
No, I’d always run. For years, I’d exercised three times a week, eaten plenty of fish, refrained from smoking and tried to keep my stress levels low. The only thing I’d changed was my intake of sugar and animal fat. 
That check-up was seven months ago and now, at 58, I’m not on a single tablet. My GP is happy. I feel better than I have in years and, at the same time, deeply concerned about proposals advising even wider use of statins. 
Until 2005, statins were prescribed only to those with at least a 30 per cent or greater risk of having a heart attack within 10 years. This was then reduced to a 20 per cent risk. Now, draft NHS guidelines would have them dished out to those with just a 10 per cent risk — in other words, most men over the age of 50 and most women over the age of 60. 
I am a vascular surgeon. Before founding a private clinic in Dorset 11 years ago, specialising in varicose veins, I worked in the NHS for 13 years. Back then, I didn’t question medical guidance on cholesterol, and thought statins were a wonder drug. And so they probably are, for men who have heart disease — not necessarily because they lower cholesterol, but because they may cut other risks such as the inflammation-marker CRP. Exercise, weight loss and omega 3 supplements also lower CRP. 
But what about other groups — women, the elderly and people like me who have not been diagnosed with heart disease? The evidence that we will benefit from cholesterol-lowering drugs is ambiguous at best. The 2011 Hunt 2 study, one of the most recent and largest, followed 52,000 men and women in Norway aged 20-74 with no pre-existing heart disease, for 10 years. 
The results for women were crystal clear. The lower a woman’s total cholesterol, the greater her risk of dying, either of heart disease or anything else, including cancer. This reflects findings in previous studies. 
For men, high cholesterol was associated with heart disease and death from other causes. But so, too, was low cholesterol — below 5mmol/l. Again, this is only an association, not a causal link. A range of between 5mmol/l and 7mmol/l was the optimum level. Guess what? This is already the national average. In addition, numerous studies have linked high cholesterol levels with increased longevity in the elderly. 
As for me, I have not been diagnosed with heart disease, and nobody in my family has had a heart attack. However, all four of my paternal uncles and my sister have diabetes. Research from Canada, published last year in the BMJ, has shown that statins raise the risk of diabetes, so that gives me little faith. The controversy over these drugs was reignited last week when Prof Sir Rory Collins from Oxford University warned that doctors’ hesitancy about prescribing them to those at risk could cost lives. 
GPs are, by definition, generalists. They don’t have time to read and analyse data from every paper on every medical condition. Even so, in a recent survey by Pulse magazine, six in 10 GPs opposed the draft proposal to lower the risk level at which patients are prescribed statins. And 55 per cent said they would not take statins themselves or recommend them to a relative, based on the proposed new guidelines. 
If that doesn’t speak volumes, I don’t know what does.