Treating insomnia naturally without medication

A lady in her early 50s had come for a repeat of her zopiclone. She had been on it for years. When I suggested a trial of cutting down, she was quite resistant. She told me she would love to if there was something else I could do to help her sleep. She told me she had tried sleep hygiene.

I said I would find out, and would see her in 4 weeks with a solution.

I searched online for studies into the non pharmacological management of insomnia. After sleep hygiene, CBT for insomnia seemed to be the best approach.

Old me: Wait. What do you mean CBT for insomnia? Like the CBT for depression?

New me: Exactly. It’s about becoming aware of the distorting effect your mind can have processing what’s really happening, and how this fighting this distorted view is what makes life difficult. NHS choices mentions a few centres which did it.

Old me: But what exactly does CBT for insomnia involve?

New me: The treatments are summarised on NICE CKS.  Most insomniacs can identify with one or more of the following patterns:

“I keep checking the clock throughout the night, and get more frustrated as I rack up sleepless hours”

“I take extra naps during the day to compensate for my problems sleeping at night”

“I lie in bed worrying that I’m not getting to sleep”

You can start by explaining a few things:

  1. Most of us get more sleep than we think we do. We remember tossing and turning and going to the toilet and checking the clock. We think this took up hours of the night. In reality, it was likely only a few seconds to minutes, but because it stays in your memory and you know 8 hours have passed overnight, on recollection your mind expands the time spent in the tossing and turning state.
  2. Had a rubbish night’s sleep? Great! This is an excellent opportunity. That could be the first step to sorting it all out. When you are really tired, stay awake. Don’t nap. Don’t go to bed early. When you finally collapse at a good bedtime, the time to onset of the first few stages of sleep is much shorter. You are basically KO’d before you get a chance to worry about the lack of sleep.
  3. There’s an interesting evolutionary theory about why we sleep at different hours through life.  Imagine a cave with young children, teenages, middle aged people and seniors. Someone has to be awake at night to guard things. Children are useless. Teenagers go to sleep late and wake up late, so are ‘on call’ for the first bit of the night. The seniors go to sleep early and wake up early, so do the early morning shift. And the middle part of the night? Well, hopefully it should be OK. But if it’s not, middle aged people have lighter sleep (i.e. are more easily woken up) so spring into action only if actually needed. Like your A&E consultant on a night shift.
  4. That wasn’t really a point about insomnia.
  5. Did you wake up in the middle of the night? It might be natural. Historically some societies also had two sleep cycles. We’re all individual; there is no set sleep pattern that you have to follow.
  6. The reason I’m mentioning all this because rigid sleep expectations is a cognitive error that leads to dissatisfaction with sleep. So don’t worry about chasing a number of hours necessarily. If you feel good in the morning and during the day, you had enough.

Old me: So what behavioural change do you suggest?

New me: The first thing I’m suggesting is Sleep Restriction. In addition to strict sleep hygiene, the patient should avoid napping or having an early night. In fact, if they need to get up at 8am, they are only allowed to sleep after midnight. They might feel more groggy for the next day or ten, but eventually they will look forward to midnight and collapsing asleep. They will be too tired to care about not getting to sleep and instead just fall asleep.

Then after a while of undisturbed sleep until the alarm rings, you can set the bedtime gradually earlier until you find a level of sleep that maintains sleeping through the night with feeling fully refreshed. Bear in mind that this number of hours is not the be all and end all. The patient should realise that they will naturally compensate for any sleep deficiency in the next sleep cycle by drifting off quicker. It’ll all work.

Old me: What are you basing this on?

New me: Most of the principles are in Overcoming Insomnia by Edinger and Carney. You can prescribe this book from the library in our practice. There’s a manual to train you and a workbook to train the patient.

Old me: And how did you choose that?

New me:  I discussed this with a sleep specialist from Sweden who had written several of the interesting papers in the field.

Old me: OK! Let’s do that now!

New me: You do that. There’s more to type up, but I’m off to sleep now. 11pm is my strict bedtime or I’ll need a nap tomorrow.


Mildy deranged LFTs in the GP setting

A man in his mid 30s was invited to make a routine appointment to discuss his LFTs.

6 months ago Now Reference range
Alanine Transferase  67 132 < 40 IU/L
Aspartate Transferase  Not done Not done < 48 IU/L
Alkaline Phosphatase  85 91 30 – 130 IU/L 
Gamma GT  43 38 < 50 IU/L in men< 35 IU/L in women
Bilirubin  16 18 < 21 µmol/L
Albumin  42 44 35 – 50 g/L


He used to drink quite heavily as a student, but was now drinking about a pint of beer every two weeks since he graduated.

He had lived in the Far East for five years, and returned to the UK two years ago. He used to use heroin and amphetamines IV whilst in the Far East. He had never received a blood transfusion.

He had never been jaundiced.

He was overweight, with a BMI of 33. His fasting glucose was 4.5. His total cholesterol was 6.6 mmol/L with HDL 0.7 mmol/L.

There was no family history of liver disease, but his father did have a coronary stent put in at the age of 40.

On examination, there were no signs of chronic liver disease, and his liver was not enlarged nor tender.

He had an US abdomen 6 months ago, which showed a diffusely fatty liver.

Old me: Bloody hell. Treat the patient, not the number. It’s just a slightly abnormal isolated LFT; these things are common.

New me: We’re probably underestimating the extent of liver disease in our general population. Most of the time (90-95%) patients with abnormal LFTs do actually have an underlying liver disease.

Of those who don’t, some have a non-liver sources for their enzymes (commonly muscle/heart for AST and bone for alkaline phosphatase).

And to make things worse, our reference range probably misses some liver disease. Lots of slow burning chronic liver disease can occur without dramatic hepatocyte death, so the intracellular enzymes from the liver that we use as markers of liver injury (AST and ALT) don’t rise so dramatically.  In South Korea, a prospective cohort study (wonderful Wikipedia diagram of how a cohort study works) involving 94 533 people found that having your AST or ALT in the upper end of the normal range was associated with having increased mortality from liver disease. The authors suggested that reducing the reference range to around 30 IU/L would pick up liver disease earlier. Does this apply in the UK? The prevalence of hepatitis B (UK: 0.3%, S. Korea 4%) and C (UK: 0.5%, S.Korea 1.3%) is lower here, but our burden of liver disease is thought to be significantly underestimated.

Old me: OK, so we should probably take it seriously. Full liver screen, see him in two weeks with the results.

New me: In this patient’s case, there is a clear risk factor for viral hepatitis. IVDU in the Far East is a dangerous game. However, if this risk factor were not present, would we still send the panel?

You should first check the patient does not have any evidence of decompensation. This means no ascites, variceal bleeding or encephalopathy. These patients may need admission.

You should also consider any acute problems leading to markedly deranged LFTs. In particular, drug-induced, ischaemia and infection can cause an acute rise in the transaminases > 1000 IU/L.

If there’s nothing too dramatic going in, you could split the possible causes into those initially treatable in GP world and those that need a referral to a Liver God. The main initially treatable ones in GP world ones are drug induced, alcohol and NASH. So if this is the first occasion of an LFT derangement, the patient is asymptomatic and the derangement is not too marked (<2x upper limit of normal), you could repeat the LFTs at 3-6 months having stopped any offending drugs (including over the counter culprits), cut down the alcohol, got the BMI below 25 and reassessed. If the LFTs have not resolved after 6 months, or if the derangement was initially marked (>2x upper limit of normal), you should proceed to a liver screen.

Old me: Drug induced, eh? This means you would stop a statin/not start him on a statin because of his LFTs.

New me: NICE (1.4.33) still recommend a baseline LFT and stopping if LFTs reach more than three times the upper limit of normal at 3 months. This will probably change eventually, and most hepatologists do not consider the transient elevation of transaminases that occurs when starting statins to be linked with liver failure. There is even evidence that NASH improves with statin therapy. This patient would benefit from a statin given his lipid profile and his family history of CV disease.

Old me: And to assess severity, its not about the degree of derangement of the liver enzymes. It’s about the functional state of the liver.

New me: Absolutely. It’s like amylase in acute pancreatitis – you get the initial organ damage and this releases an intracellular enzyme that we use for diagnosis, but not prognosis. You’ll notice that the King’s College criteria for paracetamol induced and non-paracetamol induced liver failure both ignore the transaminases and alkaline phosphatase levels. They care about the functional bits – pH and bilurubin (metabolic function), encephalopathy (detox function) prothrombin time (synthetic function) etc. The prognosis (in terms of mortality) can be estimated using the MELD score or Child Pugh score.

Old me: You do an FBC to look for a low platelet count, which goes with alcohol.

New me: Yes it does go with alcohol, for many reasons. But in terms of liver things, any chronic fibrosis can lead to portal hypertension and hypersplenism. As a result of the hypersplenism you get thromboycytopenia.

Old me: You do a liver screen to look for autoimmune, metabolic and infectious etiologies. If this is negative and the LFTs are still deranged, refer.

New me: There is information in the history and examination that cannot be obtained in the blood tests. Alcohol use is the main feature on the history. The presence of heart failure on history or examination is important too, as this can cause a congestive hepatopathy. If the liver screen is negative despite all this, an ultrasound of the abdomen can help distinguish some biliary problems and provide some information about the structure of the liver. Referral is usually done after US of the abdomen and a liver screen unless there is a clinical urgency.

According to the BSG, the liver screen should consist of:

Hepatitis B surface antigen

Hepatitis C antibody

Anti-mitochondrial antibody

Anti-smooth muscle antibody

Anti-nuclear antibody

Serum immunoglobulins (IgG can be markedly raised in autoimmune hepatitis)

Serum ferritin

Transferrin saturation

Copper and caeruloplasmin (under 40 years)

a1 antitrypsin level





Antibiotic associated diarrhoea: My new primary care strategy

A woman in her mid 50s had been prescribed doxycycline 5 days ago for persistent upper respiratory symptoms.  She returned to us because of watery diarrhoea since yesterday. There was no fever, pain or vomiting. She had eaten nothing out of the ordinary and no contacts were affected.

She was clinically well hydrated and had no other medical problems.

Old me: OMG! C diff! Admit!

New me: This is a possibility, but only 10-20% of antibiotic associated diarrhoea is caused by C diff. Most of the time the problem is an alteration in the bowel flora. The third potential mechanism is a direct prokinetic effect of the antibiotic, typically erythromycin.

Old me: Still, it’s C. diff till proven otherwise. The antibiotic must be stopped and a stool sample for C diff toxin sent.

New me: The antibiotic should ideally be stopped. Whether or not stool samples need to be sent routinely is a matter of risk. The two questions I need to ask myself are:


a)   How likely is it that in this patient there is C. diff?

b)   If it were C. diff and I missed it, how bad would that be?


a) What makes it likely to be C. diff?

This can be split into factors in the history of the presenting complaint and patient factors.

HPC: Fever, blood in stools, crampy pain and a tender abdomen go more with C diff; non C.diff antibiotic induced diarrhoea tends to be more of a ‘nuisance diarrhoea’ (not too severe).

Patient factors (according to NICE CKS):

1. Advanced age — the rate of positive C. difficile assay results in people older than 65 years of age is 20–100 times greater than the rate in people 10–20 years of age.

2. Antibiotic treatment — although none can be excluded, the most commonly implicated antibiotics are:


Cephalosporins — in particular second- and third-generation cephalosporins (such as cefuroxime axetil, cefixime, ceftriaxone, and cefotaxime)

Fluoroquinolones (such as ciprofloxacin, norfloxacin)


Ampicillin and amoxicillin (which may relate mainly to the volume of their use rather than being high risk)

3. Underlying morbidity such as abdominal surgery, cancer, chronic renal disease, and tube feeding.

4. Current use of a proton pump inhibitor (such as omeprazole and lansoprazole) or other acid-suppressive drugs (such as H2-receptor antagonists).

Two further important risk factor are hospitalisation (C diff colonisation rates of about 20-30 percent, compared to 3 percent in the general population) and previous C. diff infection. In fact, the recurrence rate is around 20% for the first infection and 45-60% after the second episode in hospitalised patients.


b) If it were C. diff, how bad would it be to miss it?

C. diff infection can cause anything from a self resolving bout of diarrhoea to pseudomembranous colitis, toxic megacolon, perforation of the colon, sepsis and death. As with any diarrhoea, there is always a risk of dehydration.


Old me: OK, so what is the mechanism of C. diff infection then?

New me: It’s not as simple as ‘take a culprit antibiotic –> kill off the good bacteria –> let C. diff proliferate’. This mechanism does not explain why C diff occurs in outbreaks on wards, as antibiotic exposure is pretty constant from week to week.

It’s like Quasar.

When I was a kid, we used to go to Quasar. If you got shot, a voice came from your gun saying ‘Defence shield active, active. Warning, warning’. The idea was that for two seconds, the defence shield was active (you could not shoot, but could not be shot) and then you were in trouble for two more seconds (you could be shot, but could not shoot). This was terrible game design. The defence shield bit was OK, but the warning bit encouraged picking on one victim over and over.

Clearly I got over this and was definitely not one of the people who got picked on over and over on at his own Quasar birthday party by his own friends.

Antibiotics put you in the ‘warning, warning’ phase. The disruption to the bowel flora is the first hit. If you then meet C. diff whilst you are in the warning, warning phase, that is the second hit. You then go one of two ways. Most people get colonised asymptomatically. A minority get C. diff infection. It’s not clear what determines your fate after the second hit, but it is probably a mixture of virulence factors and host factors.



Old me: Oh, I see. Most of the time you can tell it’s unlikely to be a C. diff infection then.

New me: Yeah. NICE CKS say that if C. diff is suspected, then get a stool sample sent. If not, don’t.

The usual rules for deciding who to admit with gastroenteritis apply. If you suspect C. diff, assess severity.

If you are going to send a stool sample for C.diff toxins, bear in mind there is a 10-20% false negative rate. Because of this, you may have to repeat the C. diff toxin test 24 hours after a negative result if clinical suspicion remains. This is because quite a bit of toxin needs to be detected to give a positive test.

Old me: What about loperamide? The BNF says absolutely no way in antibiotic-associated colitis.

New me: This caused me a problem. My patient was using loperamide, and was going on a long distance journey the next day. She wanted to know whether loperamide was safe.

Loperamide is safe in non colitis / non C. diff antibiotic associated diarrhoea However, it leads to retention of the toxin as well as potentially increasing intraluminal pressures in C. diff infection.

My patient seemed very well and clinically had ‘nuisance diarrhoea’ rather than C. diff. Not taking loperamide would clearly affect her life the next day. I advised her it should be OK as long as she is pain free, but to restrict use to during the coach journey and to keep hydrated.