Why Kegel exercises are NOT the solution to recovery of continence after prostate surgery

The idea that Kegel exercises are “the” solution to the incontinence problem is fundamentally flawed. It assumes that the stronger you make your pelvic floor muscles the better your continence gets. But this is a trap. It then implies that one has to keep doing pelvic floor exercises for the whole of one’s life, otherwise incontinence will come back again.

This is an extremely inefficient “solution”.

Instead, we need to retrain the entire muskulo-skeletal and neurological system to take on new responsibilities. We need to challenge the entire abdomen and related area to learn new way of functioniong. When the entire abdominal area reprograms itself to take on new responsibilities, we will not need to undertake any more special exercises.

This is somewhat like the child who has to learn how to become continent. The child merely pays attention to the relevant muscles and over the course of a few months becomes continent. We do not tell the child to keep exercising specific muscles. Likewise, when we do this properly, there is no need to exercise or strengthen a specific muscle after that.

I gave up Kegel exercises for roughly after the first 4 months after I realised that this was not the kind of thing I wanted to achieve. I wanted to lead my normal life without thinking about my pelvic floor.

One of my physios, Terry, showed me why retraining is important. I extrapolated and almost completely dropped all kegel exercises as soon as possible after I started jogging downhill.

So far I find that this hypothesis is correct, because I have seen continuous improvement incontinence regardless of the fact that I am no longer doing any Kegel exercises.

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What is the current state of knowledge regarding cholesterol? Small LDL particles do matter, but these reduce when you eat saturated fat.

MAIN PRINCIPLE 1: Cholesterol level (in all its complexity) is just ONE of many predictors of heart disease. Further, in most cases its impact is NOT what has been commonly known to doctors. Things are far more complicated. One must not jump to any conclusions based on any cholesterol level figures. The data need to be considered VERY CAREFULLY, and together with a large number of other factors, such as C-reactive protein and homocysteine, apolipoprotein and many others.

MAIN PRINCIPLE 2: 80 to 90 per cent of the body’s cholesterol is genetically programmed and is produced by the body. “Cholesterol is a vital component of every cell membrane on Earth. In other words, there is no life on Earth that can live without cholesterol.” [Source] + “cholesterol is one of the “most vital” molecules in the body and prevents infection, cancer, muscle pain and other conditions in elderly people.” [Source – read the paper here]. Don’t bother about cholesterol in things you eat (e.g. eggs and prawns).

The body tightly regulates the amount of cholesterol in the blood by controlling its production of cholesterol. When your dietary intake of cholesterol goes down, your body makes more. When you eat larger amounts of cholesterol, your body makes less [Source]

For six years [Indian researcher, Malhotra] had registered how many people had died from a heart attack among more than one million employees of the Indian railways. According to Malhotra’s report; employees who lived in Madras had the highest mortality. It was six to seven times higher than in Punjab, the district with the lowest mortality, and the people from Madras also died at a much younger age. People in Punjab consumed almost seventeen times more fat than people from Madras and most of it was animal fat. In addition they also smoked much more than in Madras. [Source: Uffe Ravnskov, Ignore the Awkward.: How the Cholesterol Myths Are Kept Alive]

And DO NOT CUT DOWN SATURATED FATS (but the middle path principle applies).


Uffe Ravnskov, Ignore the Awkward.: How the Cholesterol Myths Are Kept Alive

and Dr. Malcolm Kendrick’s The Great Cholesterol Con: The Truth About What Really Causes Heart Disease and How to Avoid It

And watch this:




Very little. This chart gives it all away (the white line is the FRAUDULENT line presented by a “medical scientist” to fool the world. The other numbers are the real numbers. No correlation. Mexicans consumer a large proportion of their calories from fat but have very little cardiac disease. There is tons of other data that confirms that there is NO correlation between consumption of fat (as generally understood) and heart disease.


This, too, is very weak. “After an examination of almost one thousand patients during surgery, American and world-renowned heart surgeon Michael DeBakey came up with the same message: Atherosclerosis has nothing to do with the concentration of cholesterol in the blood.” ( Garrett HA and others. JAMA 1964;189:655-9.) – cited in Uffe Ravnskov, Ignore the Awkward.: How the Cholesterol Myths Are Kept Alive


Total Cholesterol Level is NOT a Great Indicator of Your Heart Disease Risk [Source]

  • unless it is VERY high

But – HDL/TOTAL CHOLESTEROL RATIO >0.25 is good. [Source]

IS HIGH High-density lipoprotein (HDL) GOOD? NOT NECESSARILY

“according to several recent studies, good cholesterol alone has little ability to lower heart-disease risks, and more is not necessarily better.” HDL is not a very good therapeutic target,” says cardiologist Dennis Ko, a senior scientist at the Toronto-based Institute for Clinical Evaluative Sciences. What’s more, Ko’s own research suggests that above a certain threshold, more HDL could increase health risks.[Source]

IS HIGH LDL (Low-density lipoprotein) BAD? NOT NECESSARILY.

Relying on LDL-C alone can be misleading. [Source]

In fact, “older people with high LDL (low-density lipoprotein) levels, the so-called “bad” cholesterol, lived longer and had less heart disease.” [Source]

LDL type AND number of particles matters

People who have mainly large LDL particles actually have a lower risk of heart disease [Source]

Only the so-called small dense LDL particles can potentially be a problem, because they can squeeze through the lining of the arteries and if they oxidize, otherwise known as turning rancid, they can cause damage and inflammation. [Source]

High numbers of small, dense LDL particles are associated with increased risk for coronary heart disease in prospective epidemiologic studies. Subjects with small, dense particles (phenotype B) are at higher risk than those with larger, more buoyant LDL particles (phenotype A). [Source]

Blood levels of LDL-P and apolipoprotein B are strongly correlated with the risk of coronary heart disease. Both these measurements reflect the actual number of LDL-particles. A high TG/HDL-C ratio likely reflects a large number of LDL-particles


American researcher Ronald Krauss found that the most useful risk marker, the best predictor of myocardial infarction among the blood lipids, wasn’t the total amount of cholesterol in the blood, neither was it the ‘bad guy’, LDL cholesterol. It was a special type of LDL particles, the small and dense ones. The most surprising finding was that if somebody ate a large amount of saturated fat, then the number of these small, dense LDL particles decreased. [Source: Uffe Ravnskov, Ignore the Awkward.: How the Cholesterol Myths Are Kept Alive]

Trygliceride/HDL ratio is very important

Many studies have found that the triglyceride/HDL cholesterol ratio (TG/HDL-C ratio) correlates strongly with the incidence and extent of coronary artery disease. This relationship is true both for men and women. One study found that a TG/HDL-C ratio above 1.74 was the most powerful independent predictor of developing coronary artery disease.  TG/HDL-C ratio less than 0.87 is ideal.  [Source]



if you have chronic inflammation is a C-reactive protein (CRP) blood test. CRP level is used as a marker of inflammation in your arteries.

Generally speaking:

— A CRP level under 1 milligrams per liter of blood means you have a low risk for cardiovascular disease

— 1 to 3 milligrams means your risk is intermediate

— More than 3 milligrams is high risk [Source]

Also: homocysteine and apolipoprotein.

Coronary calcium scan 

The coronary calcium scan … looks at plaque in the arteries leading to the heart. Plaque in these arteries is a red flag for a potential heart attack. [Source]

Ultrasound of the carotid artery

This scan “looks at plaque in the main blood vessel leading to the brain. Plaque in the carotid artery is a sign of increased risk for a heart attack and stroke.” [Source]

Cut down infections

There is evidence that infections are associated with heart disease.


Does cholesterol matter? Cholesterol and fat myths.

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Root canal experience

I grind a lot at night. After nearly six decades one of my teeth cracked.

Root canal – stage 1 last week. X ray showed everything is OK. The first day or so the tooth felt wobbly, as if it is going to come out. That’s actually a normal thing, I gather. This feeling went away by the third day. Some pain while biting, but all sensitivity due to the crack has gone.

The crown was fitted after around two months of Stage 1, and since then there’s been no issues whatsoever. The tooth can’t be distinguished from other teeth.

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Advanced/ dynamic/ integrated Kegel exercises to curb incontinence

These are my notes from my visits to physios and readings. Unfortunately, there is no book available that documents these exercises systematically. Time permitting, I might write a book on this (plus one on RSI and one on eystrain – on which I have had a similar experience that there is lack of systematic information and I’ve had to figure out everything on my own).

NOT use glutes/ abdominal muscles/ anal muscles

The key is to focus on the two urinary muscles and avoid unnecessarily activating the anal muscle.


Use paper towel in each case to ensure you are do these till the point that you do not leak.

While lying down, pull PFM and take knee to the side, and back.

While sitting, pull PFM and rise, then release

While standing, pull PFM and sit down, then release

While standing, pull PFM then lift legs as if walking

While standing, pull PFM, then bend forward and stop

While standing, pull PFM, then cough

To prevent leaking while exercising

Dynamic Hip Flexor Stretch

Stand in a neutral position with your feet shoulder-width apart and your hands hanging naturally by your side. Lift your right foot off of the ground and take a long step forward coming into a lunge. Hold for one second before carefully coming back to the starting position. Repeat with your left leg forward and then continue alternating legs. Complete this movement for 30 seconds.

Dynamic Side Lunge Stretch

Stand with your feet hip-width apart with your toes pointed directly forward. Bring your hands together in front of your chest. Take a step to the side with your right foot. Once it’s planted, push your hips backward and bend your right knee to 90 degrees. Your left knee should stay straight as you lower into the lunge. Come up out of the lunge and then bring your right foot back to the starting position. Go right into the next repetition, this time stepping to the side with your left foot. Complete this movement for 30 seconds.


With your feet shoulder-width apart, keep your back straight, spine neutral, chest up, and your shoulders square. As you squat down, focus on keeping your knees in line with your feet. Your knees should not move in close to one another nor should they fall out to the sides. Also, you want to make sure that your shins stay as vertical as possible as you lower yourself into the squat position. Try using a chair to help you as you learn the technique. As you get stronger, you can lose the chair and start to go deeper into the squat or start doing them quite a bit faster while maintaining that good posture. Perform 3 sets of 10 repetitions.

Three-Way Lunge

With your feet shoulder-width apart, keep your back straight, spine neutral, chest up, and your shoulders square. Step forward with your right foot and bend at your knees until they both make a 90 degree angle and then step back to your starting position. Next, step to the side with your right foot. Once it’s planted, push your hips backward and bend your right knee to 90 degrees. Your left knee should stay straight as you lower into the lunge. Then return to the starting position. Finally, step backwards with your right leg so that your right knee is almost touching the floor and both knees are at a 90 degree angle. Return to the starting position and then repeat on the opposite side. Add speed to the movements in all three directions to advance the exercise. Perform 3 sets of 10 repetitions on each side.


Lie face down on the floor. Place your forearms on the floor, elbows under your shoulders. Place your legs together with balls of your feet on the floor. Lift your body off of the floor maintaining a straight line from your head through your torso to your feet. You don’t want your lower back to drop down or sag, nor do you want your butt to be high up in the air. Remember, a nice straight line. If you notice that your form starts to falter and you aren’t able to maintain the straight line, stop the exercise and rest. Perform 3 sets of holding for 15-20 seconds. Once you are able to hold for 20 seconds without losing form, try to gradually add more time to the exercise.

Keep in mind that proper posture is important with these exercises. Keep your shoulders back, your back straight, and engage your abdominal muscles throughout the exercises by drawing your belly button in toward the spine. Notable changes can be seen when you perform pelvic floor exercises every day. As your symptoms improve, you can begin a maintenance program of three times per week.

Strengthen the core to improve continence

Document – http://umuch.org/-/media/systemhospitals/uchs/pdfs/rehab/pelvicfloor.pdf?la=en&hash=F1AB321AADB45BC1EA13CA4F38E3A4AB6BB1BEC0


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My decision regarding Stage One Johanson urethroplasty for sub-meatal/ fossa navicularis urethtral stricture: A STITCH IN TIME SAVES NINE

Here’s my research and underlying arguments to go for surgery:


The fact that I now HAVE a stricture can’t be avoided. Its cause was also unavoidable. While fixing the bigger issue (cancer) this smaller issue was unavoidable, given my body’s existing anatomy.

“Distal urethral strictures confined to the fossa navicularis and meatus comprise approximately 18% of all anterior urethral strictures.”

“for whatever reason a scar develops as a consequence of changes in the structure and function of the urethral epithelium and the sub?epithelial spongy tissue causing a fibrotic narrowing of the urethra. Secondary changes in the epithelium more proximally develop there afterwards causing a progressive stricturing of an increasing length of the urethra from before backwards” [Source]

My previous notes/ research on this issue:

Tests needed before urethroplasty

Dealing with sub-meatal urethral stricture: meatoplasty and dilation (related: fossa navicularis strictures)

Complications after prostate surgery – Stricture/Bladder Neck Contracture >> Optical Urethrotomy

Injury to penis by catheter after prostate surgery/ referred pain in the penis from surgery


“Since the catheter utilized in retrograde urethrography may obscure much of the distal urethra, voiding urethrography can often provide superior radiographic assessment of the distal urethra.” [Source] [Sanjeev: In my case, the radiographer managed to get a clear image from only the use of the retrograde technique, at the very end of his process while the radioactive liquid was squirting out. The video is a bit clearer but the picture below is good enough. It clearly shows the abrupt narrowing and the location and extent (length) of the stricture:


“Distal urethral strictures confined to the meatus and fossa navicularis are particularly challenging because: (I) consideration must be given not only to establishment of durable patency of the urethra but also maintenance of glans cosmesis; and (II) these strictures are frequently related to lichen sclerosus, an inflammatory process which can cause local tissue destruction and a propensity for disease recurrence following treatment.” [Source]


“Traditionally, distal anterior urethral strictures have been treated with dilatation and internal urethrotomy, respecting the so-called reconstructive ladder. Open surgery has usually been chosen as a last option. However, it has now been realized that these minimally invasive options do not have a durable effect and may further compromise the quality of the local tissue for future reconstruction” [Source] – Management of the stricture of fossa navicularis and pendulous urethral strictures: Shrawan K. Singh, Santosh K. Agrawal, and Ravimohan S. Mavuduru, Indian J Urol. 2011 Jul-Sep; 27(3): 371–377.

“The notion that the urologist should proceed up the “reconstructive ladder”, exhausting endoscopic procedures and simple procedures before pursuing complex reconstruction has been refuted in the literature. This approach is often ineffective and does not limit patient morbidity, decrease disease progression, or minimize cost. Instead, a more prudent approach to the treatment of distal strictures is to determine which singular or staged intervention offers the patient the highest likelihood of durable patency with the least morbidity, while honoring patient-related goals. Ultimately, decision-making should be individualized, based on stricture burden, etiology, and patient motivation. [Source]- Distal urethroplasty for fossa navicularis and meatal strictures, Elodi J. Dielubanza, Justin S. Han, and Chris M. Gonzalez, Transl Androl Urol. 2014 Jun; 3(2): 163–169



“Given the dearth of evidence of long term efficacy and the potential for patient discomfort, strong consideration should be given to avoidance of dilation in favor of reconstructive approaches.” [Source]

“The clearest argument for referral for urethroplasty lies in the futility of repeat urethrotomy or dilation. Dilation is particularly unreliable. In 1949 Scardino and Hudson published the declaration that urethral dilation for stricture was “useless”. Modern series show at least an 88% failure rate for a first urethral dilation and we predict second dilations have a 100% failure rate. Somehow this concept has gotten lost with time.” [Source: Should We Centralize Referrals for Repair of Urethral Stricture? – Richard A. Santucci, Journal of Urology, The, 2009-10-01, Volume 182, Issue 4]

“Yet today alone dozens of patients worldwide will likely undergo repeat urethrotomy, and doctor and patient will hope for success that will likely never come. These are the patients who should be referred to a urologist with knowledge of urethroplasty whether near or far. For most patients referral for urethroplasty instead of additional ineffective urethrotomy should be the standard of care.”   [Source: Should We Centralize Referrals for Repair of Urethral Stricture? – Richard A. Santucci, Journal of Urology, The, 2009-10-01, Volume 182, Issue 4]

[Sanjeev: given the speed of recurrence in my case, dilation was guaranteed to fail. It is good I did not try it and have gone straight for urethroplasty after a single DVIU urethrotomy. ]


“With a flow rate of less than 5?ml/second, abnormalities such as those listed above are much more likely and the patient is potentially at risk of acute retention, although this is a lot less common than one would expect from the severity of the narrowing of the urethra that is seen in such a situation. In these patients treatment is advisable even if symptoms of voiding difficulty are not troublesome.” [Source: Management of urethral strictures, A R Mundy, Postgrad Med J. 2006 Aug; 82(970)]

My current flow rate is around 6.5 ml/ second. However, the trend in my case is VERY STRONG: a steep (but slowing) decline in the size of the opening (lumen) of the urethra. The average urine flow has reduced from over 18ml/sec 10 days after urethrotomy to an average of around 6.5 ml/sec, less than 4 weeks from the urethrotomy. The decline from 18 ml to around 6.5 has occurred in a mere two weeks.

Although the level has stabilised for around four days, it would be a delusion to imagine that the end of scarring has been reached. It is barely four weeks from urethrotomy. My flow rate is likely to quickly reduce below 5ml/ second, going into the danger zone.

The question is: should I undergo surgery at this stage or should I wait for it to get worse before finally getting the surgery done?



a) It is futile to imagine that the stricture will somehow remain at the current level. There is no evidence in the literature that strictures stabilise or disappear or settle down on their own. The probability of the stricture getting worse and needing the same (or more severe surgery) is 100 per cent. IT IS FUTILE TO THINK THAT THIS ISSUE WILL SOMEHOW “STABILISE”. For instance, I had first thought it might stabilise at 12> ml/sec, but that didn’t happen. Then I thought it might stabilise at 8-9 ml but that didn’t happen. In my case:

a) I have a particularly strong tendency to scar (as illustrated by the heavy scarring observed by the surgeon inside my abdomen at the time of the radical prostatectomy); and

b) the underlying epithelial and spongiforous tissue has clearly been affected. If left untreated, the damage could spread and lead to a LONGER stricture, making things much more difficult to treat in the future.

b) Severe damage can occur the more I delay: “More pressure is needed from the bladder muscle to pass urine out through a stricture (it acts like a bottleneck). Not all urine in the bladder may be passed when you go to the toilet. Some urine may pool in the bladder. This residual pool of urine is more likely to become infected. This makes you more prone to bladder, prostate and kidney infections. A ball of infection (an abscess) above the stricture may also develop. This can cause further damage to the urethra and tissues below the bladder. Cancer of the urethra is an extremely rare complication (Sanjeev: but not zero probability) of a long-standing stricture.” [Source]


Even in the best case (0.1 per cent chance) if the stricture stabilises, its existence will prevent any normal catheter being used in my case in the future. There will almost certainly be circumstances in my life in the future when I need a catheter – for some surgery or other. Each time that happens my existing stricture will force a major surgery to install a suprapelvic catheter. That is not just an additional cost (and pain) but an additional risk of further complications. If I can fix this issue now, I’ll be able to use a normal catheter in the future, when it becomes necessary.



Go ahead with the surgery.


    • I’m extremely fortunate that the proposed surgery HAS A VERY HIGH PROBABILITY OF FIXING the problem PERMANENTLY – since no graft is involved: only a diversion of the urethral exit point, with only the healthy portion of the urethtra being used and the rest blocked off. (If I choose to undergo Stage Two, there will be a risk of recurrence of some other scar tissue – however, that might be cosmetically and functionally desirable, and should be considered after continence is achieved: State Two should be done before ED has been sorted out. ED is fixed then there is horrible pain while a catheter is in place post-surgery (see patient’s report here). [Note: Ensure that the surgeon excises the ENTIRE damaged portion of the urethra so a clean “bed” is available for State Two, and scarring does not spread across the system]
    • One can’t escape surgery – or worse complications. Better to bite the bullet and prevent complications. The surgeon is not available again till 25 October and the other potential surgeon (whom I’d have otherwise met on 16 October) might not have had any vacancy till well into October/early November. A delay at this stage will leave me exposed to a HUGE risk of Emergency Department suprapubic catheter. That would complicate things badly, cost time and money, disrupt the incontinence recovery, AND NOT PREVENT THIS SAME (OR MORE COMPLICATED) SURGERY IN THE FUTURE. [Btw, Suprapubic catheter is no walk in the park. It causes significant pain and spasming – see patient report. And any surgery can lead to complications. The fewer the surgeries you have in your life the better. Better to bite the bullet and not ruminate.]
    • The surgery will impose minimal disruption (barely two weeks) on my attempt to regain continence.


  • There will be adjustments to make after Stage One surgery. On the other hand, if these adjustments are excessive, I can undergo Stage Two surgery. Therefore there is a further remedy available.

The decision is now crystal clear. IMMEDIATE SURGERY IS THE BEST YOU CAN DO, GIVEN THE PREVAILING STATE OF KNOWLEDGE. In the future, if you continue to live, new long term remedies might become available. The goal at this stage is to minimise further damage.


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