You have to go back to the early 1950s to be before oral drugs and of course to before 1922 to be before insulin.
Here's quite a grim article from the 1950s ( though as you can imagine, there aren't that many actually online)
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1929977/pdf/bullnyacadmed00465-0029.pdf
"The incidence of premature arteriosclerosis in the adult as measured by retinopathy, hypertension and albuminuria appears to be identical with that in the juvenile diabetic. Here, too, the earliest retinal lesions were noted about thirteen years after onset of diabetes, and associated with hypertension and albuminuria in about 50 per cent of patients.' An apparent acceleration of the lesions was typical of the mild cases in this older age group, because of the insidious undramatic onset of diabetes sothat duration of the disease could not be determined accurately. The incidence of fatal coronary disease in diabetes is twice that of non-diabetic males and triple that of non-diabetic females....
The diabetic predisposition to peripheral vascular disease is even more striking. Bell claims that on the basis of arteriosclerosis alone, gangrene develops nearly forty times more frequently in diabetic than in non-diabetic individuals..' (continues in similarly depressing manner including) ' Accelerated vascular damage which is an associated phenomenon and not a complication of diabetes appears to be related primarily to the duration of the disease; its course up to the present time has not been altered significantly by the use of insulin, the type of diet or the level of control of glycosuria and hyperglycemia.'
There were arguments about whether glycaemic control made any difference in outcome.
.Those arguments were partially resolved in that the
UKPDS (a type 2 trial) showed that tight(er) control, (not really that tight, 7% compared with 7.9% over 10 years) including the Sulfs and insulinimproved microvascular outcomes; but unfortunately there was no improvement in macrovascular outcomes.
http://www.ncbi.nlm.nih.gov/pubmed/9742976
In contrast,the
DCCT and EPIC trials in Type 1 showed benefits for both microvascular and macrovascular outcomes. (again tight control was ~7%) but with younger patients no real effect on mortality demonstated. However 8 years later they showed significant reductions in both the incidence of CVD events and death from them
The downside was that the lower HbA1cs increased the risks of serious hypoglycaemic events(ie those that needed intervention from another person)
The really good thing was that follow up over many years has showed what they call a legacy effect; this period of tight control seems to have beneficial effects in later years. The effect persists even if glucose levels rose to those of the non tight control group .
http://www.niddk.nih.gov/about-nidd...l-follow-up-study/Documents/DCCT-EDIC_508.pdf
Ten years later they also found a legacy effect in the intensive treatment arm of the UKPDS demonstrating reductions in MIs and overall mortality.
http://www.jwatch.org/jw200810140000001/2008/10/14/legacy-effect-intensive-control-type-2-diabetes
Roll forward and three fairly recent trials that looked at tight control in T2 again.
Accord; took those with long term T2, medicated them down with an aim of 6% and had to be stopped because of increased cardiovascular mortality in the intensive arm. (reduced microvascular complications though)
http://www.diapedia.org/introduction-to-diabetes-mellitus/accord
Advance: again started with people at risk of CVD; reduced levels more slowly, found no harm and slightly reduced macrovascular complications, a bigger improvement in microvascular outcomes but no reduced mortality either. So far, they have found no legacy effect for glucose control but have found that there was one for tight blood pressure control
http://www.medscape.com/viewarticle/832114
VADT: older men with high HbA1c . Again no adverse effects , lower incidence of cardiovascular events but no reduction in mortality.
http://www.medscape.com/viewarticle/845848#vp_2
The big difference between UKPDS and the later trials is I think the age and the length of time people had had T2 before the trials
(and in some cases, quite possibly the drugs used)
And you'll find lots of interpretations and reanalysis of these trials from every different viewpoint.
None of them really have much relevance to those that do not require drugs or insulin .
In the 1950s this was an option that would 'work' for fewer people than today. Most wouldn't have been diagnosed until they had had diabetes for a number of years. (even in the nineteen nineties when there was a fasting level used for diagnosis, it was higher than the fasting level used today; the HbA1c for diagnosis only came in the last couple of years)
