Can nutrition support healthy cognitive ageing

by Amy Jennings .. Senior Postdoctoral Fellow

Around 50 million people worldwide have dementia, the main form of which is Alzheimer’s disease. Dementia is a major cause of disability and dependency in older adults and, owing to expanding and ageing populations, its prevalence is expected to almost triple by 2050. This increase is being partly offset by decreasing age standardised dementia rates in some high income countries, attributed to more years of education and improved cardiovascular health.1 In England and Wales, dementia is the first and second leading cause of death in women and men, respectively, responsible for 16.3% and 8.7% of total mortality in 2017 (www.ons.gov.uk). Almost two thirds of cases of dementia are in women. The cause of this difference between the sexes is poorly understood.2

Interventions to improve cognition and reduce dementia risk
No licensed drugs are available that prevent or reverse dementia. For Alzheimer’s disease four drugs are used to treat symptoms temporarily (donepezil, rivastigmine, galantamine, and memantine). Therefore, behaviour which prevents or delays progression of neuropathology and brain vascular dysfunction could help to reduce the individual risk and population burden of the disease. The 2014 report, “The trajectory of dementia in the UK–making a difference,” estimated that a two or five year delay in the onset of dementia would reduce the number of people with the disease in the UK by 19% and 33%. respectively, by 2050.3 In a US based analysis, Brookmeyer and colleagues predicted that interventions associated with a five year delay would almost halve cases of dementia over 50 years.4

It is estimated that about one third of cases of Alzheimer’s disease worldwide are attributable to modifiable risk factors,5 many of which are nutrition and lifestyle dependent (depression, mid-life obesity, mid-life hypertension, and type 2 diabetes). Cardiometabolic health is a major determinant of age related cognition function and risk of dementia. Research into the role of nutrition in age related cognitive decline is in its relative infancy compared with other chronic conditions, such as cardiovascular diseases, type 2 diabetes mellitus, osteoporosis, and gastrointestinal disorders.

Although the results are not fully consistent,6 a growing body of prospective cohort evidence shows that bioactive components of food are associated with a reduced risk of dementia.78 Much of the research has considered dementia as a composite, despite the recognition that owing to differences in pathology, dementia subtypes (eg, Alzheimer’s disease, vascular dementia, dementia with Lewy bodies) are probably influenced by differing dietary factors. Furthermore, a large retrospective cohort study9 has shown that behaviour, including a healthy diet, partly mitigates the penetrance of a high dementia genetic risk score. Model systems have provided insight into the potential underlying molecular and physiological mechanisms for the associations observed, including improved cardiometabolic health and brain perfusion, and direct effects within the brain on neuronal function, energy metabolism, and β amyloid processing.

The randomised controlled trial evidence is more limited and less convincing,710 with cognition and brain volume (as assessed by MRI) as the main study endpoints, and few primary prevention randomised controlled trials with incident dementia as an outcome measure.

Nutrition and cognition

Some evidence suggests that individual food bioactive components protect cognitive health (for review see Scarmeas et al8), including B vitamins, antioxidant vitamins, selenium, vitamin D, medium chain triglycerides, and long chain omega-3 fatty acids (see supplementary table on bmj.com). This evidence is not conclusive, however. Any effects of intervention with such individual components are most likely to appear after long term exposure, and in those with a low baseline habitual intake. Evidence that nutrition has a beneficial effect on brain function is stronger for healthy dietary patterns, probably because the synergistic effect of several bioactive components affects many physiological processes and signalling pathways underlying cognitive function and decline. Intuitively, one would predict that the effect of nutrition would be more evident in people who are still cognitively healthy or prodromal, rather than in those with diagnosed dementia, where significant neuronal loss has already occurred, but this has not been rigorously tested.

Here we focus on fish/the omega-3 fatty acid docosahexaenoic acids (DHAs), ketogenic interventions, and a plant based dietary pattern (eg, Mediterranean diet) as approaches to nutrition with a strong potential to mitigate age related cognitive decline. The state of advancement of knowledge and inconsistencies in these areas provide insight into the research approaches used and the challenges encountered in confirming nutrition-cognition causal relations, especially during ageing.

Omega-3 fatty acids and improved brain function

Oily fish, which includes salmon, mackerel, herring, fresh tuna, and sardines, are the almost exclusive dietary source of the long chain n-3 fatty acids, eicosapentaenoic acid and docosahexaenoic acid (DHA). Algal oil capsules provide a vegan source of DHA. The brain is highly enriched in DHA, which constitutes 15% of brain lipids compared with less than 5% in most other tissues.11 The role of DHA in the developing fetal and infant brain is widely accepted. In prospective cohort studies, high fish and DHA intake has been consistently associated with improved cognitive health in older age, with a 10-30% reduced risk of Alzheimer’s disease and death, brain atrophy, and cognitive decline, and effect sizes equivalent to two to four years of ageing1213141516; there is some indication of greater effects in women.15 In a meta-analysis of 21 cohort studies, a 100 mg increment of dietary DHA was associated with lower risks of dementia (relative risk 0.86, 95% confidence interval 0.76 to 0.96) and Alzheimer’s disease (0.63, 0.51 to 0.76).14 Fish is also a source of multiple nutrients needed by the brain, including vitamin B12, selenium, and vitamin D, which may contribute to the observed cognitive benefits. Thus, where possible, fish itself rather than fish oil supplements is recommended as a source of DHA.

For a dietary component such as DHA/fish, which could be considered a signature of an overall healthy diet (such as a Mediterranean-style diet discussed below) and healthy behaviour, the possibility of residual confounding should be considered, as some of the cognitive benefits associated with DHA seen in prospective cohorts could be due to a yet unknown factor associated with intake,17 and the benefits associated with eating fish and DHA could be biased.18

A number of randomised controlled trials have reported mixed findings with DHA supplementation over periods of up to three years (see supplementary data). DHA is one of the bioactive ingredients in Souvenaid (Fortasyn Connect) medicinal food, designed to support cognitive ageing. In the LipiDiDiet trial, Souvenaid had no effect on the primary outcome measure, but was associated with an improved clinical dementia rating score and reduced hippocampal (a main brain region affected in Alzheimer’s disease) atrophy.19

Response to DHA interventions is heterogeneous and may partly depend on DHA and cognitive status at baseline. Cognitive benefits are reported for healthy younger adults20 and in mild cognitive impairment,21 in contrast to those with more advanced disease.22 Early indications are that APOE4 carriers (25% of white populations), and particularly older women with the APOE4 variant, may have lower brain DHA uptake and status, and would benefit from higher dose DHA supplementation.22324 For DHA and other dietary components, several variables need to be considered, including delivery to the brain and time taken to reach a steady state, and whether the cognitive benefits are direct effects on brain structure, perfusion, or metabolism, or an indirect effect attributable to, for example, cardiometabolic health. Brain DHA half life is estimated to be 2.5 years,25 and thus supplementation periods of at least a year are probably needed to detect the cognitive benefits associated with DHA enrichment of neuronal cells, and effects on β-amyloid and tau protein metabolism and synaptic plasticity.226

Brain glucose use, ketones, and cognitive health

One of the challenges facing the ageing brain is a chronic deficit in brain glucose uptake. Cognitively healthy older adults have about 7-8% lower brain glucose uptake than younger adults, a decline accentuated in mild cognitive impairment (the prodromal phase of Alzheimer’s disease) and even more so in Alzheimer’s disease itself.27 Although low brain glucose could be a consequence of the disease process, two facets of the declining glucose uptake, brain cell loss, cognitive decline continuum suggest that this interpretation should be reconsidered. Firstly, brain glucose uptake is already lower in those at risk of Alzheimer’s disease (that is, older age but still cognitively normal, carriers of the presenilin mutation or APOE4, or type 2 diabetes) but before their cognition declines.28

Secondly, studies with positron emission tomography imaging and a ketone tracer (11C-acetoacetate) show that, unlike glucose, brain ketone uptake is normal during ageing, mild cognitive impairment, and Alzheimer’s disease.293031 Ketones are the brain’s second most important fuel and, as for glucose, brain ketone uptake is an active, transporter mediated process. Hence, many of the brain cells in which glucose metabolism is deteriorating owing to age or Alzheimer’s disease are not apoptotic (or dead) because they can still metabolise ketones. Rather, they are gradually becoming energy (glucose) starved, but perhaps their function could be revived or maintained by ketones, an emerging therapeutic concept called “brain energy rescue”.32

Under normal circumstances, glucose supplies about 95% of the brain’s fuel. It is, however, effectively replaced by ketones (β-hydroxybutyrate and acetoacetate) when dietary carbohydrate or total dietary energy is limited. Furthermore, when a ketogenic supplement is included in the diet, the brain of someone with mild cognitive impairment or Alzheimer’s disease uses ketones in direct proportion to the increased ketones provided by the circulation, thereby sparing brain glucose use.3334

Recent experimental clinical studies have shown that brain energy rescue with ketones is associated with improved cognitive outcomes in both mild cognitive impairment and Alzheimer’s disease. These studies used either a very low carbohydrate (ketogenic) diet353637 or 20-30 g/day of ketogenic medium chain triglyceride supplement.343839 With ketone positron emission tomography imaging, two of these studies showed that not only did ketones access the brain of someone with mild cognitive impairment37 but that improvement on several cognitive tests was directly proportional to the rise in plasma ketones,34 implying a direct mechanistic link between restoration of brain energy levels by ketones and the improved cognitive performance. Ketogenic interventions may also be disease modifying because preclinical and clinical reports show that the neuropathological process involving accumulation of the dementia associated proteins, amyloid β and phosphorylated tau, can be partially blocked by ketogenic supplements.374041 These results are encouraging but compliance is low with ketogenic diets, and ketogenic medium chain triglycerides can cause gastrointestinal discomfort. Thus more work is needed to optimise ketogenic interventions (dose, duration, formulation) and test them in larger randomised controlled trials in order to convincingly assess their efficacy in improving cognitive outcomes in people with mild cognitive impairment or Alzheimer’s disease. Ketogenic interventions may indirectly affect cognitive outcomes, in part, by improving insulin sensitivity or stimulating weight loss; they would also be predicted to be more efficient in slowing down Alzheimer’s disease if combined with exercise.42 Given the emerging evidence for the cardiometabolic safety of the ketogenic diet and the growing interest in its use to treat type 2 diabetes,43 a long term controlled intervention assessing its effect on cognitive outcomes and risk of Alzheimer’s disease is warranted.

Dietary patterns and cognitive health

Recent research has moved away from the reductionist approach to nutrition, health, and chronic disease,17 and focused on the effect of dietary patterns, such as the Mediterranean diet, DASH (Dietary Approaches to Stop Hypertension) diet, and the hybrid MIND (Mediterranean-DASH Intervention for Neurodegenerative Delay) diet. Additionally, the World Health Organization and Public Health England have advocated whole diet approaches to delay or prevent cognitive decline.744 A Mediterranean diet is high in fruits, vegetables, olive oil, whole grains, unsaturated fatty acids, and fish, with restrictions of red meat, and moderate but regular drinking of alcohol. A meta-analysis of 34 168 participants showed that higher adherence to a Mediterranean diet was associated with a 21% reduced risk of developing cognitive disorders and a 40% reduced risk of Alzheimer’s disease.45 In a recent analysis of the EPIC (European Prospective Investigation into Cancer and Nutrition)-Norfolk cohort, the global cognitive benefit of high versus low adherence to a Mediterranean diet was equivalent to 1.7 fewer years of cognitive ageing.46

Numerous foods in modern Western-style diets are not traditionally included in a Mediterranean diet, such as high fat dairy products, processed meats, carbonated drinks, sweets, and pastries. The PREDIMED, MIND, and DASH diets are Mediterranean-style diets and all three improved cognitive outcomes,4748 with respectively a 53%, 54%, and 39% lower incidence of Alzheimer’s disease after 4.5 years.49 A multidomain lifestyle intervention trial (FINGER), which included modified eating behaviour as one of four concurrent interventions, improved cognitive outcomes. After two years, a 25% improvement in global cognition (as assessed by the neuropsychological test battery), and higher executive function (150%) and processing speed (89%) was evident in the intervention versus control group.5051 These findings indicate that whole diet approaches that encourage Mediterranean-style elements and discourage energy dense foods typical of a Western-style diet are beneficial for cognitive health. Although the PREDIMED study reported a lower prevalence of mild cognitive impairment after a Mediterranean diet,52 longitudinal randomised controlled trials, with incident mild cognitive impairment/Alzheimer’s disease as the primary end point, are still lacking.

The totality of evidence supports the protective effect of adherence to diets rich in whole foods for dementia and cognitive function, but there are inconsistencies within and between diets.45 Contradictory findings may be due to the geographical region, with a recent systematic review reporting that 80% of cohort studies conducted in Mediterranean regions showed significant associations with cognitive health, compared with only 50% in non-Mediterranean regions.53 Possible reasons for this geographical disparity are firstly, diet adherence scores may reflect different food patterns in Mediterranean versus non-Mediterranean countries—for example, olive oil, fish, and legumes are more commonly eaten in Mediterranean regions; secondly, adherence scores do not consider foods reflective of Western-style diets in non-Mediterranean regions; or, thirdly, in Mediterranean regions the Mediterranean diet score is “capturing” a lifestyle with characteristics protective of cognitive decline, including increased social interactions when eating, and physical activity.5455

Heterogeneity in dietary response could also be due to individual differences in nutrient metabolism. Beneficial changes in the gut microbiome, together with taxonomic shifts in microbiota composition, have been seen in those following plant based diets.56 A higher intake of plant based foods is associated with lower trimethylamine oxide levels and increased faecal short chain fatty acids, fibre degrading microbiota, and gut microbial diversity.5758 These gut microbial changes are linked to the gut-brain axis. Thus short chain fatty acids—in particular, butyrate, enhance brain derived neurotrophic factor expression, and trimethylamine oxide is linked to reduced expression of synaptic plasticity related proteins, including N-methyl-D-aspartate-receptors, both important factors for learning and memory.5960 If the microbiome can affect the gut-brain axis then diet induced changes in the gut microbiota, through plant based or Mediterranean diets associated with higher consumption of fibre, polyphenols, and probiotics could affect development of cognitive impairment. Equally, microbiome speciation and metabolism could influence the cognitive response to dietary change and may emerge as a tractable target for interventions.

In addition to the nutrients needed for brain function, the reduced content of refined sugars in Mediterranean-type diets may also help to improve glucose tolerance. This would help the ageing brain meet its energy needs (both glucose and ketones) by reducing creeping insulin resistance during ageing, thereby improving the chance of maintaining optimal cognition.

Conclusions

Prospective cohort evidence suggests that a change in eating behaviour may delay the onset of dementia, possibly by several years. The trial evidence to date is reliant on cognitive or other surrogate markers of dementia risk with often, uncertain prognostic value, and lacking sensitivity and specificity to dementia subtypes. Longitudinal randomised controlled trials with robust cognitive outcomes are still needed, ideally, with incident disease (either dementia or mild cognitive impairment) as the primary outcome. Metabolic and preclinical studies will help to provide insights into mechanisms so as to collectively provide the evidence needed to make causal inferences, fully establish efficacy, and inform policy.17 Randomised controlled trials are often expensive and long term. They should be supported by validated imaging and biochemical biomarkers of disease, both to select at risk and responsive subgroups, and to screen potentially effective interventions.

Are we yet in a position to provide dietary guidelines specifically to promote cognitive health and reduce the risk of dementia in later life? Global and national dietary macronutrient (particularly fat and carbohydrate) and food guidelines (eg, eating fruit and vegetables and reducing salt) are, in large part, based on the management of cardiometabolic risk (obesity, cardiovascular diseases, and type 2 diabetes mellitus). Given the established importance of cardiometabolic health on cognitive function (especially in mid-life), greater adherence to existing dietary recommendations is likely to reduce the incidence of dementia. To develop dietary guidelines specifically focused on prevention of dementia or improving mild cognitive decline, further research is needed to gain insight into which dietary strategies most effectively improve neuronal function and reduce neuropathology.

Controversies and research gaps

Strong associations between dietary patterns and food bioactive components in prospective cohort studies and experimental preclinical studies are often not replicated in human randomised controlled trials Randomised controlled trial design should assess whether the intervention indirectly affects systemic processes, such as cardiometabolic function or inflammation, or whether it directly affects neuronal function, brain energy metabolism, or the “hallmarks” of dementia, such as amyloid β and tau protein metabolism. The time and dose needed to produce meaningful increases in brain function must be considered in the trial design to preclude the risk of a type 2 error (false positive findings) Longitudinal follow-up randomised controlled trials are needed, ideally with incident disease as the primary outcome measure It is unclear when to intervene in the cognitive course from health to diagnosed dementia, and which interventions are best suited to dementia subtype and disease progression Little is known about the overall effect of neuropathology on the brain uptake and metabolism of dietary components Identification is needed of targeted approaches to nutrition for at risk subgroups, such as women with the APOE4 gene or insulin resistant individuals

Key messages

Global prevalence of dementia is predicted to almost triple by 2050 and no current treatments are effective Improved eating behaviour could reduce the risk and population prevalence of dementia Owing to dementia’s multifactorial aetiology, multiple dietary components that target several physiological pathways and risk factors simultaneously are needed

Changes to dietary patterns and foods (rather than single dietary components) therefore hold most promise to meaningfully improve cognition Randomised controlled trials with robust validated cognitive outcomes are needed to support the prospective cohort evidence, establish efficacy and effect size, and inform public health policy

Tell all the truth - Emily Dickinson

Tell all the truth but tell it slant —

Success in Circuit lies

Too bright for our infirm Delight

The Truth's superb surprise

As Lightning to the Children eased

With explanation kind

The Truth must dazzle gradually

Or every man be blind —

The much needed fiscal policy during covid 19 lockdown in india

There are multiple measures implemented by the government to stimulate the economy in the covid 19 induced pause in the economic activity. The question is whether they are effective and is there a magic pill which could resolve all the issues

All stimulus should have the desired effect on increased spending and resultant surge in economic activity. Unlike a developed economy, India cannot afford to provide unemployment packages like PPP (paycheck protection programme) as their tax collections are abysmally low. Indias tax to GDP ratio is c.10% as compared to US-24% UK- 34%. Also a significant majority of the labor force is outside of the payroll system in India which is evidenced by the low personnel registered for employee security schemes like EPF,NPS etc. It means that it is virtually impossible for India to have a payroll based stimulus as it would basically ignore most of the labor force.The fact that India dont have an universal health care system compounds the impact in case of surge of covid 19 cases. Thereby it is prudent for the government to have a strict lock-down to prevent a pandemic and the medical resources of State and Central Governments being overwhelmed. It provides the government a breather and focus their initiative in mitigating the constraints imposed on the economy by such strict lockdown measures.

FISCAL MULTIPLIER

Any macroeconomic study is incomplete without analysis of the desired fiscal multiplier effect of a stimulus package. It is defined by the marginal propensity to consume ("MPC") of the beneficiaries of the scheme. If the government has limited resources as is the case for India with lower tolerance for increased fiscal deficit, they should look for a package which could act like a adrenaline shot to the comatose economy.

The poor families usually tend to have the highest MPC as they usually spend most of their revenues on sustenance. It is the same essential goods and services which are allowed to operate in the lockdown. Thereby it would be an accurate assessment that any stimulus directed toward the families of the Public distribution system (PDS) i.e ration card holders below a certain level of income should have the desired impact of increased economic activity. Grocery stores also employ labor with a higher MPC thereby leading to the compounding effect of the stimulus i.e the fiscal multiplier.

CONSTRAINTS

Will the families be allowed to spend primarily on the essential goods - what if they have a outstanding loan and rental payments

The Government did announce a moratorium on rental collections but it needs to be strictly implemented and extended till the lock-down restrictions are eased. A prolonged moratorium is required on both rental and loan repayments (inc. interest) as it defeats the purpose of any benefit package if most of it used to pay a landlord or loan shark who doesnt have the desired MPC/fiscal multiplier effect.

If only essential goods and services are available then people with higher income usually tend to save as there are basically limited avenues to spend other than food during the lockdown

Thereby any benefits directly provided to individuals or families should be directed towards increased propensity to buy groceries and eliminate any redirection to leverage or rental costs.

FIRMS

The above direct stimulus to individuals through PDS or bank accounts can help to sustain the poorer section of society who are the hardest hit for a few months but what about firms. The actual engine of production for the economy, what is the impact of strict lockdown measures on them

There are three key factors which needs to be considered

a) Low margin industry - High fixed cost

b) High inventory

c) Largest employment - direct and indirect

First we need to accept that the government cannot allow a large number of firms to go bankrupt due to the govt lockdown as it would create a comatose climate which would be far more difficult to recover than the covid 19 pandemic. Thereby the Government should drive the initiative to hit the above three factors.

Any industry with high fixed cost ratio would be crippled and are most likely to go bankrupt. Even-though they can prevent working capital issues by reducing inventory or even laying off temporary staff but they cannot avoid the fixed costs like borrowing, property,plant and equipment maintenance and depreciation.

Firms carrying large unsold inventory either in the form of raw materials or finished goods would find it difficult to restart operations as the carrying cost of inventory would significantly impair their cash flows.

Large employers primarily in the manufacturing sector would require the most support as they would be the most likely to lay off permanent staff and reduce their purchase orders which would in turn precipitate a vicious cycle of supplier side unemployment who are primarily in the medium and small sector

FISCAL MEASURES

The government needs to announce a funding mechanism where the RBI directly invests in firms based on the above factors. A designated bank needs to be created under the supervision of RBI which is government funded. This "Covid 19 Bank" should extend long dated instruments carrying a reasonable coupon rate with contingent convertible and a mandatory redemption feature after 5 years. This would be the much need capital infusion required for the indian industry.

The current blanket announcement of 20 lakh crore loans targetting small and medium sector through an already struggling banking sector would only add to the ever increasing NPA issues. It is difficult for a listed banking institution to carry such higher risk on their balance sheet even if it is guaranteed by the RBI/Govt due to the higher capital costs associated with the same and its resultant impact on capital ratios.

Thereby this stimulus needs to be extended by the government directly through its segregated "covid 19 bank" rather than putting the onus on the banking sector. also there is no point in targetting small and medium enterprises as evidenced in the manufacturing sector they are usually engaged in the supplier or distribution side of large enterprises. If the orders from large enterprises dry up then there is no point of any stimulus. It is imperative that we target firms based on the above three key factors and target them for covid 19 financing instruments.

Usually financing for Large industries would help them to maintain their purchase orders and also meet the sale orders when demand picks up post easing of lockdown which brings us to the next important point ...... timing.

TIMING

The above fiscal measures shouldnt be implemented at the same time. Cause there is an inherent synergy between lockdown, stimulus and increased demand. In the initial phase of intense lockdown where only essential goods and services are allowed to operate, the focus should be on the fiscal multiplier stimulus like direct money transfer to high MPC families through the PDS and banking infrastructures with strict implementation of rent and loan moratorium which needs to be extended till the end of lockdown.

During the next phase of the lockdown when the restrictions are eased for industries to operate with minimal or reduced capacity, the first tranche of funding through the Covid 19 bank needs to be extended to firms based on the above three key factors. It is important that the funding is extended in a staggered manner which is coinciding with the gradual easing of the lockdown. There is no point in a giving a bulk amount to an enterprise with no vision on when they will have the opportunity to restart their operations.

This staggered cash flow funding which is in effect a capital instrument would provide the much needed breathing space for the industry to meet the increased demand on the projected consumption post lockdown.

In case there is extended lock-down due to non flattening of the covid 19 spread then the above industry fiscal stimulus needs to be on hold.

To reiterate i believe the following key features are required to restart the Indian economy

a) Immediate and regular stimulus to PDS families during lockdown.

b) Strict implementation of Rent and Loan payment holidays during lockdown

c) A Separate Covid 19 bank created with govt funding under the supervision of RBI

d) Staggered funding timed with the easing of lockdown of long dated instruments with contingent convertible and mandatory redemption feature after 5 years

e) Targeted funding to firms based on the three key factors

The Power of Retained Earnings

In 1924, Edgar Lawrence Smith, an obscure economist and financial advisor, wrote Common Stocks as Long Term Investments, a slim book that changed the investment world. Indeed, writing the book changed Smith himself, forcing him to reassess his own investment beliefs.

Going in, he planned to argue that stocks would perform better than bonds during inflationary periods and that bonds would deliver superior returns during deflationary times. That seemed sensible enough. But Smith was in for a shock.

His book began, therefore, with a confession: “These studies are the record of a failure – the failure of facts to sustain a preconceived theory.” Luckily for investors, that failure led Smith to think more deeply about how stocks should be evaluated.

For the crux of Smith’s insight, I will quote an early reviewer of his book, none other than John Maynard

Keynes: “I have kept until last what is perhaps Mr. Smith’s most important, and is certainly his most novel, point. Well-managed industrial companies do not, as a rule, distribute to the shareholders the whole of their earned profits.

In good years, if not in all years, they retain a part of their profits and put them back into the business. Thus there is an element of compound interest (Keynes’ italics) operating in favour of a sound industrial investment. Over a period of years, the real value of the property of a sound industrial is increasing at compound interest, quite apart from the dividends paid out to the shareholders.”

And with that sprinkling of holy water, Smith was no longer obscure.

It’s difficult to understand why retained earnings were unappreciated by investors before Smith’s book was published. After all, it was no secret that mind-boggling wealth had earlier been amassed by such titans as Carnegie, Rockefeller and Ford, all of whom had retained a huge portion of their business earnings to fund growth and produce ever-greater profits. Throughout America, also, there had long been small-time capitalists who became rich following the same playbook.

Nevertheless, when business ownership was sliced into small pieces – “stocks” – buyers in the pre-Smith years usually thought of their shares as a short-term gamble on market movements. Even at their best, stocks were considered speculations. Gentlemen preferred bonds.

Though investors were slow to wise up, the math of retaining and reinvesting earnings is now well understood. Today, school children learn what Keynes termed “novel”: combining savings with compound interest works wonders.

**********

An extract from Warren Buffet's letter to shareholders of Berkshire Hathaway in annual report 2019.

Lack of testing lead to patients being discharged with Covid 19 infections

Many patients in hospitals with covid-19 may have been discharged to care homes in March and April because of a lack of testing capacity at the time in England, auditors have reported.

The National Audit Office said that actions taken by the NHS to increase capacity meant there were enough beds and respiratory support nationally at the peak of the outbreak in April.1 Actions included postponing elective procedures, contracting with private hospitals to secure extra beds, and advising hospitals on 17 March to urgently discharge all inpatients who were medically fit to leave.

But the watchdog said that the government’s testing strategy led to some patients being discharged to care homes without being tested for covid-19 between mid-March and mid-April.

The NAO reported: “Due to government policy at the time, not all patients were tested for covid-19 before discharge, with priority given to patients with symptoms. On 15 April, the policy was changed to test all those being discharged into care homes. It is not known how many patients discharged to care homes had covid-19 at the point they left hospital.” Before the new policy of testing everyone before their admission to care homes was rolled out, around 25 000 people were discharged from NHS hospitals to care between 17 March and 15 April, the NAO said.

The auditors highlighted government guidance from 2 April that stated that care homes needed to make their full capacity available and that they could admit patients with covid-19. But it said there was a lack of data on “the extent to which care homes successfully isolated staff with confirmed or suspected covid-19.”

The NAO noted that testing of care workers with symptoms was not rolled out on 15 April. And it wasn’t until 28 April that all care home staff were eligible for tests, and the health department capped the daily number of care home tests at 30 000, to be shared among staff and residents. Testing of NHS staff with symptoms was also delayed but started on 27 March.

Until mid-April the government’s policy was to test no more than five residents with symptoms in any one care home. On 11 May the health department announced that, of around 400 000 care home residents, more than 45 000 had been tested by health protection teams. But it is not known how many residents have had covid-19, the NAO concluded.

Around 5900 care homes in England (38%) reported an outbreak of covid-19 between 9 March and 17 May, the NAO said. This peaked at just over 1000 homes in the first week of April, with some regions such as the North East more affected than others.

The NAO said it had also heard concerns from a range of health and social care organisations about the supply of personal protective equipment (PPE), with central sources up to mid-May meeting only around half of the modelled requirement.

Gareth Davies, the head of the NAO, said, “While we have not sought to evaluate government’s response in this report, our work raises some important considerations.

“Government’s ability to increase beds, ventilators, PPE, and testing has varied in part because of the number of other bodies, both national and international, with which it has had to engage. All of these issues need to be taken into account as the government plans for the later phases of the pandemic and future emergencies.”

Has Sweden’s controversial covid-19 strategy been successful?

Sweden has stood out in the global pandemic by eschewing lockdown and seemingly aiming for herd immunity. Heba Habib reports that Sweden’s public was supportive of the strategy, but is now paying a heavy price.

For months Swedish public health authorities have defended their controversial decision not to lock down the country in response to the global covid-19 pandemic. Schools were closed to children under 16 and gatherings of more than 50 people were discouraged, but bars, restaurants, and other public spaces remained open, and citizens were trusted to distance themselves.

At the heart of the government’s strategy was the implicit and controversial idea that, rather than contain the spread of disease, a country could achieve herd immunity by allowing a proportion of the population to be infected—at the expense of deaths among the vulnerable. “They did not want to put it bluntly, but seeking herd immunity was always inherent in the Swedish strategy,” says Anders Bjorkman, a professor of infectious diseases at the Karolinska Institute in Stockholm.

Herd immunity occurs when a large section of the population (generally considered to be between 50% and 90% depending on how contagious the infection is1) becomes immune to a disease or virus, therefore stopping its spread. This occurs when people have enough antibodies to repel the virus—either through having been exposed to the virus and survived, or through vaccination. Advocates claimed that the Swedish approach would be more sustainable in the long run than other countries’ harsher measures. And at first it seemed to be working.

Speaking at a press conference on 26 April, Anders Tegnell, the epidemiologist credited with the Swedish strategy, said that the rise in infections was beginning to flatten and had reached a plateau in Stockholm—the centre of the Swedish outbreak—as well as in other parts of the country.

As case numbers proliferated around the world and death tolls rose in neighbouring European countries, Swedish experts, and indeed the public, still seemed largely supportive of the strategy. According to a poll conducted between 17-19 April by independent agency Novus, 73% of 1000 respondents said they trusted the strategy of the Public Health Agency of Sweden.

But time has told a different story.

Explosive numbers
Sweden has the largest number of cases and fatalities in Scandinavia—around 37 000 confirmed cases at the time of writing, compared with its neighbours Denmark, Norway, and Finland which have 12 000, 8000, and 7000 cases, respectively. All three neighbouring countries adopted a lockdown approach early in the pandemic, which they are now slowly lifting. All three have since re-opened their borders, but not to Sweden.

Sweden recorded the most coronavirus deaths per capita in Europe in a seven day average between 25 May and 2 June. The country’s mortality rate was 5.29 deaths per million inhabitants a day (the UK ranked second with 4.48) according to Our World In Data,2 an online research publication based at the University of Oxford.

And what of herd immunity? An ongoing nationwide study conducted by the Public Health Agency of Sweden on 20 May found that just 7.3% of Stockholm residents had developed covid-19 antibodies by late April—and that was the largest number of positive results found in the country.

“It means that just like other European cities in hard hit countries, it will take a long time before the majority of the population has gone through the infection and are likely immune,” said Tove Fall, professor in epidemiology at Uppsala University.

On 11 May, the World Health Organization said that global studies had found antibodies in only 1-10% of the global population, with similar findings emerging from Spain and France. The agency warned against any country depending on herd immunity as a strategy.

Backlash

“I think we’re starting to see that the Swedish model maybe wasn’t the smartest,” said former state epidemiologist Annika Linde in a 19 May interview with newspaper Dagens Nyheter.3

More than half the deaths in Sweden have occurred in care homes for older people, something Tegnell has admitted is a “failure,” especially since a cornerstone of the strategy was protecting those over 70.

Anders Vahlne, a professor of virology at Karolinska, thinks that government advice misinformed the public by implying that those who don’t have symptoms are not contagious (the Public Health Agency of Sweden’s website states “as long as siblings or other members of the family do not show symptoms of disease they can go to school, preschool, or their workplace.”). “I think this amongst other things has caused a lot of older people in care homes to get sick and die and it’s quite unnecessary,” Vahlne told The BMJ.

IVO, the Health and Social Care Inspectorate, reported4 that 75% of the complaints it had received from the public and from care workers were about the lack of protective equipment such as facemasks in care homes. One care home worker, speaking anonymously, told The BMJ that “staff often work for 14 hours with substandard protection and continue working despite exhibiting symptoms.” The guidelines keep changing in accordance with the availability of material, they added.

“One should have known what poor preparedness we had in both healthcare and care of older people,” said Linde. “A lockdown could have given us a chance to prepare, think things through, and minimise the spread of infection.”

More worryingly, Swedish doctors have expressed alarm over the matter-of-factness with which authorities seem to be treating the plight of older and vulnerable people.

Yngve Gustafsson, professor of geriatric medicine at Umea University, noted that the proportion of older people in respiratory care nationally was lower than at the same time a year ago, despite people over 70 being the worst affected by covid-19. He expressed concern about the increasing practice of doctors recommending by telephone a “palliative cocktail” for sick older people in care homes.

“Older people are routinely being given morphine and midazolam, which are respiratory-inhibiting,” he told the Svenska Dagbladet newspaper,5 “It’s active euthanasia, to say the least.”

Last chance
Jon Tallinger, a specialist in general medicine and operations manager at a hospital in Tranås, believes that Sweden’s high death toll, particularly among older people, has less to do with the covid-19 strategy and is more a consequence of decades of privatising the healthcare system.

“The power has been taken away from the doctors and healthcare specialists and given to politicians,” Tallinger told The BMJ, “So now municipalities lack the resources to save the lives of older people and those at risk.” He added that thousands of lives could be saved if people in care homes with the virus received oxygen supplies. “Older people die because they do not receive the treatment they need.”

The government insists that Sweden’s high per capita death toll can’t be attributed to the lack of a lockdown. In a press conference on 29 May, Tegnell said the comparisons were unfair as “other countries are not reporting the actual death rates. Sweden is the best in the world in reporting the actual number of dead.” The government has given no indication that it will change its strategy beyond a ramping up of testing.

Yet even on that, Tove Fall said, “What is not so much discussed so far, is why Sweden is among the worst countries in Europe when it comes to testing.” According to Our World in Data, Sweden had carried out 23.64 tests per 1000 people as of 24 May, compared with 31.59 in the UK, 31.88 in Finland, and 44.75 in Norway.

Until April, only high priority groups—patients in hospital, high risk groups such as people over 70 or with underlying conditions, healthcare staff, and key workers—were being tested, and even then only those with severe symptoms. Minister of health Lina Hallgren pledged to increase to 100 000 tests per week by mid-May, but the government has fallen far short of that goal—recent numbers ranged from 28 000 to 33 000—sparking criticism from opposition party members and even the prime minister Stefan Lofven.6

Anders Tegnell said in a 3 June press conference that there had initially been problems with laboratory capacity “but also healthcare capacity because testing is a very complicated chain of events. You need to have staff and resources in each part of the chain.” He said that while the laboratory issue had now been fixed, the resources and training are still lacking.

Fall said the restricted and low levels of testing could have consequences for tracing and isolation efforts, and that this problem isn’t being prioritised by the authorities. “Testing of symptomatic cases in the population has not been done if the patient is not in need of hospital care or is not a healthcare worker,” said Fall. “Right now, recommendations for isolation of cases are based on symptoms only, and no household quarantine is recommended.”

Meanwhile, contact tracing has been largely abandoned since the beginning of March. This despite the fact that, according to Carina King, an epidemiologist at the Karolinska Institute, Sweden is very well positioned for contact tracing thanks to its commonplace digital identity system used to access public services and more.

Remorse?

On 2 June, Anders Tegnell was interviewed by Sverige Radio, and admitted there was “quite obviously a potential for improvement in what we have done.”6
Yet in a separate interview with the Dagens Nyheter, he said he still believed the basic strategy had “worked well.” “I do not see what we would have done completely differently,” he said, “Based on the knowledge we had then, we feel we made the appropriate decisions.”
“Other countries started with a lot of measures all at once,” he told Sverige Radio, “The problem with that is that you don’t really know which of the measures you have taken is most effective.”

“If we were to encounter the same disease again, knowing exactly what we know about it today, I think we would settle on doing something in between what Sweden did and what the rest of the world has done.”

Footnotes Competing interests: I have read and understood BMJ policy on declaration of interests and have no relevant interests to declare.
Provenance and peer review: Commissioned; not externally peer reviewed